The DOI matches its Crossref record; 152 of the 152 references it cites were found in a registry or an index; none of the 131 sources its claims cite is checked for support yet.
The Two Faces of Reactive Oxygen Species in Cancer
Open accessAbstract
Reactive oxygen species (ROS), now appreciated for their cellular signaling capabilities, have a dual role in cancer. On the one hand, ROS can promote protumorigenic signaling, facilitating cancer cell proliferation, survival, and adaptation to hypoxia. On the other hand, ROS can promote antitumorigenic signaling and trigger oxidative stress–induced cancer cell death. To hyperactivate the cell signaling pathways necessary for cellular transformation and tumorigenesis, cancer cells increase their rate of ROS production compared with normal cells. Concomitantly, in order to maintain ROS homeostasis and evade cell death, cancer cells increase their antioxidant capacity. Compared with normal cells, this altered redox environment of cancer cells may increase their susceptibility to ROS-manipulation therapies. In this review, we discuss the two faces of ROS in cancer, the potential mechanisms underlying ROS signaling, and the opposing cancer therapeutic approaches to targeting ROS.
Overview
AI snapshot
Written from the paper’s full text.
TL;DR
Reactive oxygen species (ROS) have dual roles in cancer: they can promote protumorigenic signaling and also trigger antitumorigenic oxidative stress–induced cancer cell death. Cancer cells increase both ROS production and antioxidant capacity, creating an altered redox environment that may make them vulnerable to ROS-manipulation therapies.
Key findings
- Cancer cells often have increased ROS production and increased ROS scavenging compared with normal cells; this altered redox state maintains ROS homeostasis to support proliferation, survival, and hypoxia adaptation while avoiding cell death.
- ROS promote protumorigenic signaling by oxidizing and inactivating phosphatases such as PTEN and PTP1B, activating PI3K/Akt/mTOR and MAPK/ERK pathways, stabilizing HIF-1α, and supporting NF-κB/NRF2 signaling, angiogenesis, and metastasis; mitochondrial O2− from complexes I, II, and III is among 10 mitochondrial sites of O2− production implicated in redox signaling.
- Excessive ROS activate ASK1/JNK and ASK1/p38 signaling to induce cell cycle arrest, senescence, and cancer cell death; p53 loss or mutation, observed in more than 50% of human cancers, can permit ROS accumulation and protumorigenic signaling.
- Therapeutic strategies include decreasing ROS with antioxidants or mitochondria-targeted antioxidants, and increasing ROS with pro-oxidants or antioxidant inhibitors; a screen of 635,000 small molecules identified three compounds that suppress complex III O2− production and prevent HIF-1α stabilization.
Methods
- Narrative review synthesizing published literature on ROS generation, regulation, signaling, and therapeutic targeting in cancer; no primary experimental data are presented.
- Discusses mechanistic studies, mouse models, cancer cell lines, clinical trial results, and chemical screens, but does not describe a systematic search strategy, sample size, or formal quantitative analysis.
Limitations
- The paper states that dietary antioxidant supplementation has shown mixed results, with some large prospective clinical studies reporting increased cancer incidence, and that NRF2 inhibitor development is challenged by specificity.
- The paper notes that normal cells, particularly stem cells, are sensitive to ROS levels, so therapies must selectively target antioxidant pathways used by cancer cells.
- Evident from the text: as a narrative review, it lacks systematic search criteria, risk-of-bias assessment, and quantitative synthesis; many therapeutic claims rest on preclinical models and cited studies rather than new primary data.
Model-written summary. Check it against the paper before relying on it.
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Claims the paper makes
97 Not checked yet · 12 Own interpretation
None of the sources cited for this claim have been checked yet.
In the paper
“H2O2 is the best described signaling molecule”
§ The Two Faces of Reactive Oxygen Species in Cancer > ROS GENERATION AND REGULATION > Types of ROS
What the sources say
- Not checked yetcites Finkel 2011
- Not checked yetcites Reczek & Chandel 2015
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“Signaling-associated ROS are produced from two main sources, the mitochondria and membrane-bound NADPH oxidases (NOXs)”
§ The Two Faces of Reactive Oxygen Species in Cancer > ROS GENERATION AND REGULATION > Sources of ROS
What the sources say
- Not checked yetcites Brewer et al. 2015
- Not checked yetcites Goncalves et al. 2015
plainstates a cause- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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None of the sources cited for this claim have been checked yet.
In the paper
“NRF2 has been shown to be essential for cancer cell proliferation and tumorigenesis”
§ The Two Faces of Reactive Oxygen Species in Cancer > ROS GENERATION AND REGULATION > Regulation of ROS
What the sources say
- Not checked yetcites DeNicola et al. 2011
- Not checked yetcites Jaramillo & Zhang 2013
- Not checked yetcites Satoh et al. 2013
boostedstates a cause- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“tumor suppressor loss can diminish ROS elimination”
§ The Two Faces of Reactive Oxygen Species in Cancer > ROS GENERATION AND REGULATION > Regulation of ROS
What the sources say
- Not checked yetcites Schieber & Chandel 2014
plainstates a cause- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Compared with normal cells, this altered redox environment of cancer cells may increase their susceptibility to ROS-manipulation therapies.”
§ The Two Faces of Reactive Oxygen Species in Cancer > Abstract
What the sources say
- Not checked yetcites Gorrini et al. 2013b
hedgedstates a possible cause- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
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In the paper
“NRF2 constitutive upregulation has been observed in many cancer types, including skin, breast, prostate, and lung”
§ The Two Faces of Reactive Oxygen Species in Cancer > ROS GENERATION AND REGULATION > Regulation of ROS
What the sources say
- Not checked yetcites No et al. 2014
plainstates an association- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“The tumor suppressor p53 has been shown to suppress ROS accumulation by regulating the expression of a variety of antioxidant genes, including SOD2, GPX1, and CAT”
§ The Two Faces of Reactive Oxygen Species in Cancer > ROS GENERATION AND REGULATION > Regulation of ROS
What the sources say
- Not checked yetcites Kruiswijk et al. 2015
plainstates a cause- Asserted: passes — The authors put it forward as true.
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In the paper
“Therefore, the fate of ROS as a signaling molecule or toxic agent depends on the type of ROS, its local concentration, and the abundance of antioxidants”
§ The Two Faces of Reactive Oxygen Species in Cancer > ROS GENERATION AND REGULATION > Sources of ROS
What the sources say
- Not checked yetcites Chandel & Tuveson 2014
plainstates a cause- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“tumor suppressors may serve an antioxidant function in normal cells”
§ The Two Faces of Reactive Oxygen Species in Cancer > ROS GENERATION AND REGULATION > Regulation of ROS
What the sources say
- Not checked yetcites Gorrini et al. 2013a
- Not checked yetcites Tao et al. 2010
- Not checked yetcites Kruiswijk et al. 2015
hedgedstates a possible cause- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
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In the paper
“the loss of NRF2 reduces tumor burden by promoting oxidative stress–induced cancer cell death”
§ The Two Faces of Reactive Oxygen Species in Cancer > ROS GENERATION AND REGULATION > Regulation of ROS
What the sources say
- Not checked yetcites DeNicola et al. 2011
plainstates a cause- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- It may state two separate claims as one. 26
- Probably not a substantial claim. 3
In the paper
“ROS homeostasis is required for normal cell survival and proper cell signaling.”
§ The Two Faces of Reactive Oxygen Species in Cancer > ROS GENERATION AND REGULATION > Regulation of ROS
What the sources say
- Not checked yetcites Sena & Chandel 2012
plainstates a cause- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Although oncogene activation, enhanced metabolism, and hypoxia can increase ROS production”
§ The Two Faces of Reactive Oxygen Species in Cancer > ROS GENERATION AND REGULATION > Regulation of ROS
What the sources say
- Not checked yetcites Schieber & Chandel 2014
plainstates a cause- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Excessive levels of ROS can increase oxidative stress and induce cancer cell death”
§ The Two Faces of Reactive Oxygen Species in Cancer > INTRODUCTION
What the sources say
- Not checked yetcites Nogueira et al. 2008
- Not checked yetcites Trachootham et al. 2006
plainstates a cause- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“ROS accumulation can occur because ROS production is increased or ROS elimination is decreased”
§ The Two Faces of Reactive Oxygen Species in Cancer > ROS GENERATION AND REGULATION > Regulation of ROS
What the sources say
- Not checked yetcites Trachootham et al. 2009
plainstates a cause- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“On the one hand, ROS can promote protumorigenic signaling, facilitating cancer cell proliferation, survival, and adaptation to hypoxia. On the other hand, ROS can promote antitumorigenic signaling and trigger oxidative stress–induced cancer cell death.”
§ The Two Faces of Reactive Oxygen Species in Cancer > Abstract
plainstates a cause- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“when p53 is lost or mutated, as observed in more than 50% of human cancers, ROS accumulation can occur, allowing for protumorigenic signaling and cellular transformation”
§ The Two Faces of Reactive Oxygen Species in Cancer > ROS GENERATION AND REGULATION > Regulation of ROS
What the sources say
- Not checked yetcites Levine & Oren 2009
plainstates a possible cause- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“ROS also oxidize and inactivate MAPK phosphatases, inducing growth factor receptor activation and MAPK/ERK pro-proliferative signaling”
§ The Two Faces of Reactive Oxygen Species in Cancer > ROS PROMOTE PROTUMORIGENIC SIGNALING
What the sources say
- Not checked yetcites Seth & Rudolph 2006
- Not checked yetcites Son et al. 2011
plainstates a cause- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“This mechanism, termed redox relay, is a two-step process in which the scavenging enzyme (e.g., PRX or GPX) receives H2O2 oxidation and transfers the oxidation to the target protein.”
§ The Two Faces of Reactive Oxygen Species in Cancer > ROS AS SIGNALING MOLECULES > H2O2-Dependent Signal Transduction
What the sources say
- Not checked yetcites Winterbourn 2013
- Not checked yetcites Sobotta et al. 2015
plainstates a cause- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“the complete disruption of the mitochondrial respiratory chain, which reduces ROS, has been shown to diminish tumorigenesis”
§ The Two Faces of Reactive Oxygen Species in Cancer > ROS PROMOTE PROTUMORIGENIC SIGNALING
What the sources say
- Not checked yetcites Weinberg et al. 2010
plainstates a cause- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“oncogenic Kras-derived mROS activated NF-κB through PKD1 to upregulate pro-proliferative EGFR signaling, leading to the formation of pancreatic precancerous lesions”
§ The Two Faces of Reactive Oxygen Species in Cancer > ROS PROMOTE PROTUMORIGENIC SIGNALING
What the sources say
- Not checked yetcites Liou et al. 2016
plainstates a cause- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“ROS promote tumor angiogenesis and metastasis, interrelated processes often associated with a poor prognosis.”
§ The Two Faces of Reactive Oxygen Species in Cancer > ROS PROMOTE PROTUMORIGENIC SIGNALING
plainstates a cause- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“When ROS levels are too high, cell cycle arrest, senescence, and cancer cell death can occur”
§ The Two Faces of Reactive Oxygen Species in Cancer > ROS PROMOTE ANTITUMORIGENIC SIGNALING
What the sources say
- Not checked yetcites Ichijo et al. 1997
- Not checked yetcites Moon et al. 2010
plainstates a possible cause- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Inactivating mutations in p38 and JNK pathway components have been observed in numerous human tumors, suggesting that these signaling pathways promote cancer cell death”
§ The Two Faces of Reactive Oxygen Species in Cancer > ROS PROMOTE ANTITUMORIGENIC SIGNALING
What the sources say
- Not checked yetcites Han & Sun 2007
- Not checked yetcites Kennedy & Davis 2003
hedgedstates a cause- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Although the increase in ROS allows for localized signaling to promote cancer cell proliferation and survival, the increase in ROS scavenging reduces distant ROS-mediated oxidative damage and maintains ROS homeostasis”
§ The Two Faces of Reactive Oxygen Species in Cancer > TARGETING ROS FOR CANCER THERAPY
What the sources say
- Not checked yetcites Chandel & Tuveson 2014
plainstates a cause- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“As tumor cells detach from the extracellular matrix and invade the basement membrane, ROS levels increase and the reduced pool of GSH decreases”
§ The Two Faces of Reactive Oxygen Species in Cancer > ROS PROMOTE ANTITUMORIGENIC SIGNALING
What the sources say
- Not checked yetcites Schafer et al. 2009
plainstates a cause- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
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It may state two separate claims as one.
In the paper
“the small molecule piperlongumine, identified from an unbiased screen, enhanced ROS levels and the selective cell death of cancer cells by diminishing the abundance of reduced GSH”
§ The Two Faces of Reactive Oxygen Species in Cancer > TARGETING ROS FOR CANCER THERAPY > Increasing ROS Levels to Promote Oxidative Stress–Induced Cancer Cell Death
What the sources say
- Not checked yetcites Raj et al. 2011
plainstates a cause- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“The mitochondria-targeted O2− scavenger MitoTEMPO has been shown to block tumor cell migration and inhibit spontaneous tumor metastasis in human and murine models”
§ The Two Faces of Reactive Oxygen Species in Cancer > TARGETING ROS FOR CANCER THERAPY > Decreasing ROS Levels to Prevent Cancer Cell Proliferation
What the sources say
- Not checked yetcites Porporato et al. 2014
boostedstates a cause- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
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It may state two separate claims as one.
In the paper
“the mitochondria-targeted antioxidant MitoQ reduced the formation of Kras-driven pancreatic precancerous lesions, suggesting that mROS propagates the protumorigenic signal”
§ The Two Faces of Reactive Oxygen Species in Cancer > TARGETING ROS FOR CANCER THERAPY > Decreasing ROS Levels to Prevent Cancer Cell Proliferation
What the sources say
- Not checked yetcites Liou et al. 2016
hedgedstates a cause- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Because cancer cells have elevated ROS levels compared with normal cells, they are potentially more vulnerable to oxidative stress–induced cell death by ROS-producing strategies.”
§ The Two Faces of Reactive Oxygen Species in Cancer > TARGETING ROS FOR CANCER THERAPY > Increasing ROS Levels to Promote Oxidative Stress–Induced Cancer Cell Death
hedgedstates a possible cause- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“buthionine sulfoximine (BSO), an inhibitor of glutamate cysteine ligase (GCL), the enzyme required for GSH synthesis, depletes GSH and exhibits anticancer activity”
§ The Two Faces of Reactive Oxygen Species in Cancer > TARGETING ROS FOR CANCER THERAPY > Increasing ROS Levels to Promote Oxidative Stress–Induced Cancer Cell Death
What the sources say
- Not checked yetcites Andringa et al. 2006
- Not checked yetcites Bailey et al. 1997
- Not checked yetcites Griffith & Meister 1979 source
plainstates a cause- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“For example, CD44v-expressing human gastrointestinal CSCs have been shown to stabilize the cysteine-glutamate exchange transporter and increase the synthesis of GSH (Ishimoto et al. 2011).”
§ The Two Faces of Reactive Oxygen Species in Cancer > TARGETING ROS FOR CANCER THERAPY > Increasing ROS Levels to Promote Oxidative Stress–Induced Cancer Cell Death
What the sources say
- Not checked yetcites Ishimoto et al. 2011
plainstates a cause- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“a recent high-throughput screen of 635,000 small molecules against mitochondrial H2O2 production revealed three compounds that specifically suppress complex III O2− production and prevent HIF-1α protein stabilization without impairing the bioenergetic function of the mitochondria”
§ The Two Faces of Reactive Oxygen Species in Cancer > TARGETING ROS FOR CANCER THERAPY > Decreasing ROS Levels to Prevent Cancer Cell Proliferation
What the sources say
- Not checked yetcites Orr et al. 2015
plainstates a cause- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
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It may state two separate claims as one.
In the paper
“It is possible that dietary antioxidants do not efficiently scavenge the pool of protumorigenic signaling ROS and instead promote tumor progression by decreasing the toxicity of ROS distant from their site of production”
§ The Two Faces of Reactive Oxygen Species in Cancer > TARGETING ROS FOR CANCER THERAPY > Decreasing ROS Levels to Prevent Cancer Cell Proliferation
What the sources say
- Not checked yetcites Chandel & Tuveson 2014
hedgedstates a possible cause- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“a high dose of the antioxidant vitamin C has been shown to function as a pro-oxidant (ROS generator), genotype-selective anticancer agent, inducing the cell death of Kras- and Braf-mutant colon cancer cells”
§ The Two Faces of Reactive Oxygen Species in Cancer > TARGETING ROS FOR CANCER THERAPY > Increasing ROS Levels to Promote Oxidative Stress–Induced Cancer Cell Death
What the sources say
- Not checked yetcites Yun et al. 2015
plainstates a cause- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Moreover, targeting the antioxidant CAT in combination with ROS-generating CDK4 and CDK6 inhibitors has been shown to elevate ROS levels above the threshold and reduce pancreatic ductal adenocarcinoma cell growth (Franco et al. 2016).”
§ The Two Faces of Reactive Oxygen Species in Cancer > TARGETING ROS FOR CANCER THERAPY > Increasing ROS Levels to Promote Oxidative Stress–Induced Cancer Cell Death
What the sources say
- Not checked yetcites Franco et al. 2016
plainstates a cause- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“LCS-1 impaired the integrity of the mitochondria in breast cancer cell lines, but not in nontumorigenic cell lines, suggesting SOD1 inhibition as a potential therapeutic approach for breast cancer (Papa et al. 2014).”
§ The Two Faces of Reactive Oxygen Species in Cancer > TARGETING ROS FOR CANCER THERAPY > Increasing ROS Levels to Promote Oxidative Stress–Induced Cancer Cell Death
What the sources say
- Not checked yetcites Papa et al. 2014
plainstates a cause- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“During serine starvation, HCT116 p53-null cancer cells displayed impaired proliferation, decreased levels of GSH, and increased intracellular ROS levels compared with their serine-starved wild-type counterparts (Maddocks et al. 2013).”
§ The Two Faces of Reactive Oxygen Species in Cancer > TARGETING ROS FOR CANCER THERAPY > Increasing ROS Levels to Promote Oxidative Stress–Induced Cancer Cell Death
What the sources say
- Not checked yetcites Maddocks et al. 2013
plainstates an association- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“A better understanding of the molecular mechanisms of ROS signaling in cancer and the identification of specific ROS targets may provide novel therapeutic avenues for treating cancer.”
§ The Two Faces of Reactive Oxygen Species in Cancer > CONCLUSIONS
hedgedstates a possible cause- Asserted: passes — The authors put it forward as true.
- Checkable: fails — It may be too vague to check against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. It may be too vague to check against evidence.
In the paper
“Additionally, it may be beneficial to combine ROS-producing agents with ROS-scavenging inhibitors to reduce cancer cell adaptation and resistance to chemotherapeutics (Weinberg & Chandel 2015).”
§ The Two Faces of Reactive Oxygen Species in Cancer > TARGETING ROS FOR CANCER THERAPY > Increasing ROS Levels to Promote Oxidative Stress–Induced Cancer Cell Death
What the sources say
- Not checked yetcites Weinberg & Chandel 2015
hedgedstates a possible cause- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim.
The paper relies on this without support.
Protumorigenic signaling occurs near the site of ROS production.
“Because protumorigenic signaling occurs near the site of ROS production, the use of antioxidants or inhibitors that target the source of ROS generation may prevent tumorigenesis.”
The paper relies on this without support.
Cancer cells have higher levels of ROS production compared with normal cells.
“Furthermore, although initially counterintuitive, pro-oxidant cancer therapy—whereby ROS production is increased or ROS scavenging is decreased, or both—is an attractive approach, given the higher levels of ROS production in cancer cells compared with normal cells.”
The paper relies on this without support.
ROS has a causal role in promoting tumorigenesis.
“Given the causal role of ROS in promoting tumorigenesis and the widely held belief that antioxidants are tumor suppressors, ROS-manipulation strategies have previously focused on antioxidant therapy.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“ROS can either (i) promote protumorigenic signaling supporting the proliferation and survival of cancer cells or (ii) conversely promote antitumorigenic signaling and oxidative stress-induced cancer cell death (Reczek and Chandel 2017).”
From Reactive Oxygen Species, Toxicity, Oxidative Stress, and Antioxidants: Chronic Diseases and Aging (2023) · cites this paper as Reczek and Chandel 2017
Citations
Cites
2 retracted
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Raj, L., Ide, T., Gurkar, A. U., Foley, M. A., Schenone, M., Li, X., Tolliday, N. J., Golub, T. R., Carr, S. A., Shamji, A. F., et al. (2011) · Nature · doi:10.1038/nature10167 · Cited by 1,040 · cited 17×
“Additionally, it is conceivable that the thiol-containing compounds GSH or reduced TRX recycle the oxidized scavenger back to its reduced state and transmit the signal to the target protein (Shao et al. 2014).”
BackgroundInfluentialRetractedAdhikary, A., Mohanty, S., Lahiry, L., Hossain, D. M. S., Chakraborty, S., & Das, T. (2009) · FEBS Letters · doi:10.1016/j.febslet.2009.10.081 · Cited by 79 · cited 1×
“Thus, perturbing these ROS-mitigating pathways may be a viable therapeutic approach for suppressing cancer cell proliferation and metastasis (Adhikary et al. 2010, Wu et al. 2010).”
BackgroundRetractedHow mitochondria produce reactive oxygen species
Murphy, M. P. (2009) · Biochemical Journal · doi:10.1042/bj20081386 · Cited by 8,207 · cited 2×
“O2− is released into the mitochondrial matrix by complexes I, II, and III, where SOD2 rapidly converts it to H2O2 (Murphy 2009).”
BackgroundThe NOX Family of ROS-Generating NADPH Oxidases: Physiology and Pathophysiology
Bedard, K., & Krause, K.-H. (2007) · Physiological Reviews · doi:10.1152/physrev.00044.2005 · Cited by 6,989 · cited 1×
“Although primarily localized to the plasma membrane, NOXs can be found on other membranes, including those of the nucleus, mitochondria, and endoplasmic reticulum (Bedard & Krause 2007).”
BackgroundROS function in redox signaling and oxidative stress
Schieber, M., & Chandel, N. S. (2014) · Current Biology · doi:10.1016/j.cub.2014.03.034 · Cited by 6,931 · cited 2×
“Although oncogene activation, enhanced metabolism, and hypoxia can increase ROS production, tumor suppressor loss can diminish ROS elimination (Schieber & Chandel 2014).”
BackgroundSelf-citationTargeting HIF-1 for cancer therapy
Semenza, G. L. (2003) · Nature Reviews Cancer · doi:10.1038/nrc1187 · Cited by 6,717 · cited 1×
“However, during hypoxia, the HIF-α protein is allowed to dimerize with the HIF-β subunit and translocate to the nucleus to induce expression of proangiogenic genes, such as vascular endothelial growth factor and genes involved in cell survival, glycolysis, and metastasis (Semenza 2003, 2012).”
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Ames, B. N., Shigenaga, M. K., & Hagen, T. M. (1993) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.90.17.7915 · Cited by 5,958 · cited 1×
“Because high levels of ROS can cause damage to lipids, proteins, and DNA, it was thought that ROS were oncogenic, promoting genomic instability and tumorigenesis (Ames et al. 1993).”
BackgroundThe phosphoinositide 3-kinase pathway
Cantley, L. C. (2002) · Science · doi:10.1126/science.296.5573.1655 · Cited by 5,621 · cited 1×
“Thus, the ROS-induced PI3K/Akt survival pathway has been shown to be activated in a majority of cancers (Cantley 2002).”
BackgroundTargeting cancer cells by ROS-mediated mechanisms: a radical therapeutic approach?
Trachootham, D., Alexandre, J., & Huang, P. (2009) · Nature Reviews Drug Discovery · doi:10.1038/nrd2803 · Cited by 5,452 · cited 1×
“ROS accumulation can occur because ROS production is increased or ROS elimination is decreased (Trachootham et al. 2009).”
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“This results in an increase in NADPH generation and maintenance of the cellular antioxidant capacity to counterbalance the hypoxia-induced increase in mitochondrial ROS (mROS) (Kim et al. 2006, Ye et al. 2014).”
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Items 201–300 of 592
Gnocchi, D., Sabbà, C., & Mazzocca, A. (2023) · Biochimie · doi:10.1016/j.biochi.2023.01.005 · Cited by 23
Vișan, S., Şoriţău, O., Tatomir, C. B., Baldasici, O., Bălăcescu, L., Bălăcescu, O., MUNTEAN, P. A. L., Gherasim, C., & Pintea, A. (2023) · Molecules · doi:10.3390/molecules28114486 · Cited by 22
Antitumor activity of α‐pinene in T‐cell tumors
Abe, M., Asada, N., Kimura, M., Fukui, C., Yamada, D., Wang, Z., Miyake, M., Takarada, T., Ono, M., Aoe, M., et al. (2024) · Cancer Science · doi:10.1111/cas.16086 · Cited by 22
“44 Chemotherapeutic agents used to treat leukemia, such as doxorubicin and vincristine, increase ROS levels in leukemic cells.”
BackgroundChattopadhyay, M., Kodela, R., Santiago, G., Le, T. T. C., Nath, N., & Kashfi, K. (2020) · Biochemical Pharmacology · doi:10.1016/j.bcp.2020.113857 · Cited by 22
“Induction of reactive oxygen species (ROS) is also known to inhibit cell growth and induce apoptosis and cell death [11, 12].”
BackgroundElectrochemical (bio)sensors for cancer therapy monitoring
Singh, S., Glovi, A., Miglione, A., Cimmino, W., Iula, G., Antonelli, L., Cesaris, M. G. D., Felli, N., Martinelli, C. V., Laurentiis, M. D., et al. (2025) · Electrochimica Acta · doi:10.1016/j.electacta.2025.146929 · Cited by 23
Porto, V., Buceta, D., Domínguez, B., Carneiro, C., Borrajo, E., Fraile, M., Davila‐Ferreira, N., Arias, I. R., Blanco, J. M., Blanco, M. C., et al. (2022) · Advanced Functional Materials · doi:10.1002/adfm.202113028 · Cited by 23
Dong, Q., Wang, J., Liu, J., Zhang, L., Xu, Z., Kang, Y., & Xue, P. (2023) · Advanced Healthcare Materials · doi:10.1002/adhm.202301453 · Cited by 22
Spiky Silver–Iron Oxide Nanohybrid for Effective Dual-Imaging and Synergistic Thermo-Chemotherapy
Moonshi, S. S., Vazquez‐Prada, K. X., Tang, J., van Holthe, N. J. W., Cowin, G., Wu, Y., Nguyen, D. H. T., Mckinnon, R., Bulmer, A. C., & Ta, H. T. (2023) · ACS Applied Materials & Interfaces · doi:10.1021/acsami.3c04696 · Cited by 21
The impact of aneuploidy on cellular homeostasis
Newman, D. L., Thurgood, L. A., & Gregory, S. L. (2019) · Free Radical Research · doi:10.1080/10715762.2019.1623398 · Cited by 21
Kasiri, S., Chen, B., Wilson, A. N., Reczek, A., Mazambani, S., Gadhvi, J. G., Noel, E., Marriam, U., Mino, B., Lü, W., et al. (2020) · Oncogene · doi:10.1038/s41388-020-1224-5 · Cited by 21
Natural product corynoline suppresses melanoma cell growth through inducing oxidative stress
Yi, C., Li, X., Chen, S., Liu, M., Lü, W., & Ye, X. (2020) · Phytotherapy Research · doi:10.1002/ptr.6719 · Cited by 23
“ROS can promote tumor-promoting signal pathways, facilitating cancer cell survival and proliferation (Reczek & Chandel, 2017).”
BackgroundTuning the Toxicity of Reactive Oxygen Species into Advanced Tumor Therapy
Xie, A., Li, H., Hao, Y., & Zhang, Y. (2021) · Nanoscale Research Letters · doi:10.1186/s11671-021-03599-8 · Cited by 21
Reactive oxygen species in health and disease
Ren, Y., Li, J., & Dai, X. (2026) · Molecular Biomedicine · doi:10.1186/s43556-026-00419-2 · Cited by 27
“In contrast, non-radical ROS are more stable and can diffuse across membranes via aquaporins, which permits long-range, compartment-to-compartment communication [4, 5], with signaling specificity conferred by structured relay systems like the peroxiredoxin-thiore-doxin (PRX-Trx) axis [6–8].”
Tempeh extract reduces cellular ROS levels and upregulates the expression of antioxidant enzymes
Surya, R., Romulo, A., & Suryani, Y. (2021) · Food Research · doi:10.26656/fr.2017.5(3).560 · Cited by 24
“…ability to maintain ROS homeostasis to hyperactivate signalling pathways necessary for tumorigenesis, one of which is the expression of protective cellular antioxidant enzymes to tackle oxidative stress such as superoxide dismutase (SOD) and catalase (Reczek and Chandel, 2017; Wang et al., 2018).”
BackgroundXu, J., Wang, Y., Wang, Y., Wang, Z., & He, X. (2021) · Chemico-Biological Interactions · doi:10.1016/j.cbi.2021.109648 · Cited by 20
The preventive and therapeutic potential of native Brazilian fruits on colorectal cancer
do Nascimento, R. D. P., Reguengo, L. M., Machado, A. P. D. F., & Maróstica, M. R. (2022) · Food Bioscience · doi:10.1016/j.fbio.2021.101539 · Cited by 20
Zidan, A., Saadany, A. A. E., Maghraby, G. M. E., Abdin, A. A., & Hedya, S. E. (2023) · Toxicology and Applied Pharmacology · doi:10.1016/j.taap.2023.116448 · Cited by 20
Zhu, W., & Oteiza, P. I. (2023) · Redox Biology · doi:10.1016/j.redox.2023.102827 · Cited by 20
“NOX1 activation, increased oxidant production and EGFR activation can lead to the upregulation of MMPs which can then promote tumor metastasis [20,25,26].”
BackgroundConditional Control of Universal CAR T Cells by Cleavable OFF-Switch Adaptors
Kvorjak, M., Ruffo, E., Tivon, Y., So, V., Parikh, A. B., Deiters, A., & Lohmueller, J. J. (2023) · ACS Synthetic Biology · doi:10.1021/acssynbio.3c00320 · Cited by 24
Targeting the PHF8/YY1 axis suppresses cancer cell growth through modulation of ROS
Wu, X., Li, J.-Y., He, Q., Li, B., He, Y., Pan, X., Wang, M., Sang, R., Ding, J.-C., Gao, X., et al. (2024) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.2219352120 · Cited by 20
Ghotaslou, A., Azizsoltani, A., Baghaei, K., & Alizadeh, E. (2024) · Heliyon · doi:10.1016/j.heliyon.2024.e29333 · Cited by 20
Izu, G. O., Njoya, E. M., Tabakam, G. T., Nambooze, J., Otukile, K. P., Tsoeu, S. E., Fasiku, V. O., Adegoke, A. M., Erukainure, O. L., Mashele, S. S., et al. (2024) · Antioxidants · doi:10.3390/antiox13040456 · Cited by 20
“ROS may induce pro-tumorigenic signaling, which may promote cancer cell proliferation and survival [7].”
BackgroundLee, S., Lee, S. A., Shinn, J., et al. (2024) · International Journal of Nanomedicine · doi:10.2147/ijn.s460468 · Cited by 20
Loung, C.-Y., Fernando, W., Rupasinghe, H. P. V., & Hoskin, D. W. (2019) · Molecules · doi:10.3390/molecules24183335 · Cited by 20
“In line with evidence that neoplastic cells are more sensitive to ROS than are their non-malignant counterparts [23], we found that MDA-MB-231 breast cancer cells were more sensitive to ROS than non-malignant MCF-10A mammary epithelial cells.”
BackgroundGüiza, F. M., Bueno-Duarte, Y., Méndez‐Sánchez, S. C., & Bohórquez, A. R. R. (2019) · Medicinal Chemistry Research · doi:10.1007/s00044-019-02363-z · Cited by 21
Hu, T., Pan, C., Zhang, T., Ni, M., Wang, W., Zhang, S., Chen, Y., Wang, J., & Fang, Q. (2022) · Cancer Gene Therapy · doi:10.1038/s41417-022-00501-1 · Cited by 19
“At the same time, oxidative stress has also been considered to be associated with the occurrence and development of cancer [47].”
Retractedde Castro, D. T. H., Leite, D. F., Baldivia, D. D. S., dos Santos, H. F., Balogun, S. O., Silva, D. B., Carollo, C. A., Souza, K. D. P., & dos Santos, E. L. (2023) · Pharmaceuticals · doi:10.3390/ph16070951 · Cited by 18
“This finding points to a potential therapeutic strategy against cancer because the increase in intracellular ROS in tumor cells intensifies signaling death pathways such as caspase-3 activation [64,66].”
BackgroundPuiu, M., Istrate, O.-M., Mirčeski, V., et al. (2023) · Analytical Chemistry · doi:10.1021/acs.analchem.3c02919 · Cited by 19
Jeon, S., & Kim, M. (2019) · Chemico-Biological Interactions · doi:10.1016/j.cbi.2019.108826 · Cited by 19
Immunoglobulin expression in the endoplasmic reticulum shapes the metabolic fitness of B lymphocytes
Jumaa, H., Cagánová, M., McAllister, E. J., Hoenig, L., He, X., Saltukoglu, D., Brenker, K., Köhler, M., Leben, R., Hauser, A. E., et al. (2020) · Life Science Alliance · doi:10.26508/lsa.202000700 · Cited by 19
Liu, L., Cui, H., & Xu, Y. (2020) · Frontiers in Genetics · doi:10.3389/fgene.2020.00494 · Cited by 19
“…or a few molecular species such as O 2 or H + , there are many types of oxidizing molecules such as reactive oxygen species (Barash et al., 2010; Reczek and Chandel, 2017), reactive nitrogen species (Fionda et al., 2016; Kruk and Aboul-Enein, 2017), reactive lipid species (Higdon et al., 2012;…”
BackgroundFleszar, M. G., Fortuna, P., Zawadzki, M., Kosyk, B., & Krzystek‐Korpacka, M. (2020) · Molecules · doi:10.3390/molecules25215158 · Cited by 21
“When sustained, however, it can cause damage to macromolecules and contribute to the initiation and progression of a number of diseases, including cancer [1,2].”
BackgroundMapanao, A. K., Sarogni, P., Santi, M., Menicagli, M., Gonnelli, A., Zamborlin, A., Ermini, M. L., & Voliani, V. (2022) · Biomaterials Science · doi:10.1039/d2bm00994c · Cited by 18
Ferroptosis, Acyl Starvation, and Breast Cancer
Bobiński, R., Dutka, M., Pizon, M., Waksmańska, W., & Pielesz, A. (2022) · Molecular Pharmacology · doi:10.1124/molpharm.122.000607 · Cited by 20
“…or unfavorable to their growth, depending on whether they are exposed to moderate or excessive levels of stress and the internal mechanisms of both antioxidant protection and the stress defenses of the tumor (Harris, 2002; Ackerman and Simon, 2014; Manda et al., 2015; Reczek and Chandel, 2017).”
Anticancer therapeutic effect of ginsenosides through mediating reactive oxygen species
Li, X., Cao, D., Sun, S., & Wang, Y. (2023) · Frontiers in Pharmacology · doi:10.3389/fphar.2023.1215020 · Cited by 21
“these cells more susceptible to redox manipulation or altered ROS levels than normal cells (Gorrini et al., 2013; Reczek and Chandel, 2017).”
BackgroundInfluentialSingh, K., & Gautam, P. K. (2023) · BMC Cancer · doi:10.1186/s12885-023-11674-9 · Cited by 21
Abbasi, A., Pakravan, N., & Hassan, Z. M. (2020) · Journal of Cellular Physiology · doi:10.1002/jcp.29957 · Cited by 19
“However, preclinical studies on murine cancer models indicated that the therapy can promote tu- mour growth and metastasis (Habtetsion et al., 2018; Reczek & Chandel, 2017; F. Weinberg et al., 2019).”
BackgroundSilva, A. L. G., de Carvalho, N. V., Paterno, L. G., de Moura, L. D., Filomeno, C. L., de Paula, E., & Báo, S. N. (2021) · Cancer Nanotechnology · doi:10.1186/s12645-021-00083-x · Cited by 19
“…of the involvement of ROS in the regulation of numerous signaling pathways that control important biological processes related to the promotion and progression of carcinogenesis, such as migration, differentiation, proliferation and even adaptation to oxidative stress (Reczek and Chandel 2017).”
BackgroundInfluentialA reactive oxygen species-triggerable theranostic prodrug system
Liu, F., Liu, L., Wei, P., & Yi, T. (2024) · Journal of Controlled Release · doi:10.1016/j.jconrel.2024.10.054 · Cited by 17
Li, X., Yu, W., Zhang, Y., Zhao, H., Wang, J., Sun, M., Xing, D., & Wang, C. (2025) · Coordination Chemistry Reviews · doi:10.1016/j.ccr.2025.217097 · Cited by 19
Paun, R. A., Dumut, D. C., Centorame, A., Thuraisingam, T., Hajdúch, M., Mistrík, M., Džubák, P., Sanctis, J. B. D., Radzioch, D., & Tabrizian, M. (2022) · Pharmaceutics · doi:10.3390/pharmaceutics14030640 · Cited by 16
“It was recently shown that CuET can cause a conformational lock of the p97-NPL4 complex under oxidative conditions, which are elevated in cancer cells [48,49].”
BackgroundSowińska, M., Szeliga, M., Morawiak, M., Zabłocka, B., & Urbańczyk-Lipkowska, Z. (2022) · Biomolecules · doi:10.3390/biom12081116 · Cited by 17
“, [63,64] or inducing cancer-cell apoptosis [3–5,53,54,65].”
Amaldoss, M. J. N., Pandžić, E., Koshy, P., Kumar, N., Sorrell, C. C., & Unnikrishnan, A. (2022) · Methods · doi:10.1016/j.ymeth.2022.08.005 · Cited by 18
NEK6 Regulates Redox Balance and DNA Damage Response in DU-145 Prostate Cancer Cells
Pavan, I. C. B., Basei, F. L., Severino, M. B., Silva, I. R. E., Issayama, L. K., Mancini, M. C. S., Góis, M. M., da Silva, L. G. S., Bezerra, R. M. N., Simabuco, F. M., et al. (2023) · Cells · doi:10.3390/cells12020256 · Cited by 19
“Usually, cancer cells have higher levels of ROS compared to normal cells [26].”
BackgroundYin, N., Wang, Y., Qin, G., Wang, M., Tang, J., Yao, X., Xu, Q., & Yoon, J. (2024) · Sensors and Actuators B Chemical · doi:10.1016/j.snb.2024.136419 · Cited by 17
Deepak, K., Shee, M., Roy, P., & Mandal, M. (2026) · Cell Death · doi:10.1016/j.celld.2026.100009 · Cited by 19
Ferroptosis: A novel therapeutic strategy and mechanism of action in glioma
Zhang, G., Fang, Y., Li, X., & Zhang, Z. (2022) · Frontiers in Oncology · doi:10.3389/fonc.2022.947530 · Cited by 18
“However, excessive ROS accumulation promotes antitumor signaling, triggers oxidative stress, and induces cell death (58).”
BackgroundMitochondrial Metabolism Drives Low-density Lipoprotein-induced Breast Cancer Cell Migration
Pereira, S. N., Santos, F. G. D. A., Santos, M. O., et al. (2023) · Cancer Research Communications · doi:10.1158/2767-9764.crc-22-0394 · Cited by 16
Immunometabolism: a new dimension in immunotherapy resistance
Xiao, C., Xiong, W., Xu, Y., Zou, J. P., Zeng, Y., Liu, J., Peng, Y., Hu, C., & Wu, F. (2023) · Frontiers of Medicine · doi:10.1007/s11684-023-1012-z · Cited by 18
Bildik, G., Gray, J. P., Mao, W., Yang, H., Özyurt, R., Orellana, V. R., Wever, O. D., Carey, M. S., Bast, R. C., & Lü, Z. (2024) · Autophagy · doi:10.1080/15548627.2023.2299516 · Cited by 16
“Concomitantly, in order to maintain ROS homeostasis and evade cell death, cancer cells increase their antioxidant capacity [25].”
BackgroundEffect of punicalagin on the autophagic cell death in triple-negative breast cancer cells
Bhutta, Z. A., Go, R., & Choi, K. (2024) · Toxicological Research · doi:10.1007/s43188-024-00246-z · Cited by 17
“Activation of JNK is maintained by its phosphorylation by ROS [47].”
Pagano, M., Mosca, L., Vitiello, F., et al. (2020) · Cancers · doi:10.3390/cancers12123665 · Cited by 16
“Recently, it was reported that ROS generation induced by various antitumor agents is partly linked to ER-stress activation [31], indicating that there is a mutual relationship between ER stress and ROS accumulation.”
BackgroundWang, S. X., Wen, X., Bell, C., & Appiah, S. S. (2018) · Molecular Medicine Reports · doi:10.3892/mmr.2018.8396 · Cited by 16
“ROS production occurs during normal metabolic functions such as respiration (42) and the detoxification of xenobiotics.”
BackgroundJahani, M., Shahlaei, M., Norooznezhad, F., Miraghaee, S., Hosseinzadeh, L., Moasefi, N., Khodarahmi, R., Farokhi, A., Mahnam, A., & Mansouri, K. (2020) · Archives of Medical Research · doi:10.1016/j.arcmed.2019.12.002 · Cited by 15
Begines, P., Sevilla-Horrillo, L., Puerta, A., Puckett, R. L., Bayort, S., Lagunes, I., Maya, I., Padrón, J. M., López, Ó., & Fernández‐Bolaños, J. G. (2020) · Pharmaceuticals · doi:10.3390/ph13110358 · Cited by 17
“Thus, on the one hand, they can facilitate cell proliferation by acting as signalling molecules, a capacity that is increased by rising ROS levels, and a concomitant improved antioxidant machinery; nevertheless, on the other hand, ROS can also provoke cell death by inducing apoptosis [59].”
BackgroundThe Complex Roles of Redox and Antioxidant Biology in CancerPreprint
Hayashi, M., Okazaki, K., Papgiannakopoulos, T., & Motohashi, H. (2024) · Cold Spring Harbor Perspectives in Medicine · doi:10.1101/cshperspect.a041546 · Cited by 16
Periodic Exposure of Plasma-Activated Medium Alters Fibroblast Cellular Homoeostasis
Bhartiya, P., Kaushik, N., Nguyen, L. N., Bekeschus, S., Masur, K., Weltmann, K., Kaushik, N. K., & Choi, E. H. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23063120 · Cited by 17
“Elevated RONS levels act as double-edged swords involved with cellular regulatory functions ranging from stimulating cell proliferation to inhibition by inducing cell death [21].”
BackgroundBovine Lactoferrin Induces Cell Death in Human Prostate Cancer Cells
Rocha, V. P., Campos, S. P. D. C., Barros, C. A., et al. (2022) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2022/2187696 · Cited by 15
“Detection of oxidative stress was carried out using DHE, a fl uorescent probe used to detect ROS, as it undergoes a nonspeci fi c oxidation process [46].”
Frtús, A., Smolková, B., Uzhytchak, M., Lunová, M., Jirsa, M., Petrenko, Y., Dejneka, A., & Lunov, O. (2023) · ACS Biomaterials Science & Engineering · doi:10.1021/acsbiomaterials.2c01518 · Cited by 15
Self-Illuminating Near-Infrared Chemiluminescence Nanosensors for Tumor Imaging
Wang, M., Liu, R., Li, J., Zhang, Z., Yang, Y., & Wang, X. (2024) · ACS Applied Nano Materials · doi:10.1021/acsanm.4c02654 · Cited by 15
Virus/Host Cell Crosstalk in Hypoxic HPV-Positive Cancer Cells
Hoppe‐Seyler, K., Mändl, J., Adrian, S., Kuhn, B. J., & Hoppe‐Seyler, F. (2017) · Viruses · doi:10.3390/v9070174 · Cited by 16
“This can culminate in more aggressive cancer growth and higher therapeutic resistance (reviewed in [69,77]).”
BackgroundAdvances in Purpurin 18 Research: On Cancer Therapy
Pavlíčková, V. S., Škubník, J., Jurášek, M., & Rimpelová, S. (2021) · Applied Sciences · doi:10.3390/app11052254 · Cited by 16
“However, ROS play a dual role in cancer treatment, since they can trigger multiple c llular cascades leading also to pro-tumorigenesis [27].”
BackgroundSousa, C., Duarte, D., Lima, B. S., et al. (2021) · Nutrition and Cancer · doi:10.1080/01635581.2021.1955285 · Cited by 15
“It is the cell’s response to intra- and extracellular environment alterations, with a critical role in signaling pathways and homeostasis (16, 21).”
BackgroundJuriga, D., Kálmán, E. É., Tóth, K., et al. (2022) · Gels · doi:10.3390/gels8020065 · Cited by 15
“It is well known that degradation of dopamine produces reactive oxygen species (ROS) [73], which can promote cell migration by redox regulation of key signaling pathways [74], or enhances migration of tumor cells, and thereby the invasion and metastasis of cancer [75].”
BackgroundGreenwood, H. E., Edwards, R. S., Koglin, N., Berndt, M., Baark, F., Kim, J., Firth, G., Khalil, E., Mueller, A., & Witney, T. H. (2022) · Theranostics · doi:10.7150/thno.63237 · Cited by 14
“A consequence of the greater metabolic demand of cancer cells to sustain increased proliferation compared to non-transformed cells is the increased production of reactive oxygen species (ROS) in the mitochondria [14, 15].”
Harris, A. R., Esparza, S., Azimi, M. S., Cornelison, R., Azar, F. N., Llaneza, D. C., Belanger, M. C., Mathew, A. S., Tkachenko, S., Perez, M. J., et al. (2022) · Frontiers in Oncology · doi:10.3389/fonc.2022.801764 · Cited by 12
“Platinums have been shown to increase ROS (35), and ROS can lead to enhanced proliferation, survival, and inflammatory pathways (36), all of which we observed in our LECs”
BackgroundVrdoljak, N. (2022) · Critical Reviews™ in Oncogenesis · doi:10.1615/critrevoncog.2022045331 · Cited by 15
Notaro, A., Lauricella, M., Liberto, D. D., Emanuele, S., Giuliano, M., Attanzio, A., Tesoriere, L., Carlisi, D., Allegra, M., BLASIO, A. D., et al. (2023) · Antioxidants · doi:10.3390/antiox12061292 · Cited by 14
“The fine-tuning of some anti-neoplastic therapies that promote an escalated ROS generation that overwhelms the scavenging tumor ability seems to be the other side of the coin that could be exploited as an Achilles’ heel and drive tumors to different death pathways, such as apoptosis, autophagy or necroptosis [61].”
BackgroundOm, H., Chand, U., & Kushawaha, P. K. (2023) · Cancer Immunology Immunotherapy · doi:10.1007/s00262-023-03551-y · Cited by 15
“…increase the expression of antioxidants like superoxide dismutases (SOD), catalase (CAT), glutathione peroxidases (GPXs), peroxiredoxins (PRXs); genes involved in NADPH production; utilization genes and glutathione (GSH) synthesis; and detoxification enzymes to balance ROS inside cancer cells [59].”
BackgroundOmran, M. M., Kamal, M. M., Ammar, Y. A., Abusaif, M. S., Ismail, M. M. F., & Mansour, H. H. (2024) · Scientific Reports · doi:10.1038/s41598-024-69250-5 · Cited by 15
“Because pro-tumorigenic signaling occurs near the site of ROS production, the use of antioxidants or inhibitors that target this source of ROS creation may prevent carcinogenesis 35 .”
BackgroundOxidative State in Cutaneous Melanoma Progression: A Question of Balance
Benedusi, M., Lee, H., Lim, Y., & Valacchi, G. (2024) · Antioxidants · doi:10.3390/antiox13091058 · Cited by 16
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“signaling pathways necessary for their survival, proliferation, andmetastasis (Reczek and Chandel, 2017).”
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BackgroundInfluential
Metadata
- Authors
- Reczek, C. R., & Chandel, N. S.
- Affiliations
- Northwestern University (US)
- Venue
- Annual Review of Cancer Biology
- Publisher
- Annual Reviews
- Published
- 2017-03-06
- Volume
- 1
- Issue
- 1
- Pages
- 79-98
- ISSN
- 2472-3428 (ISSN-L)
- PMC
- PMC11875389
- OpenAlex
- W2509946779
- Semantic Scholar
- fa6f060895b44afc150511174ef31fd04137e66e
- Cited by
- 602
- References
- 151
- Citations by year
- 2026: 72 · 2025: 50 · 2024: 55 · 2023: 78 · 2022: 134 · 2021: 97 · 2020: 53 · 2019: 37 · 2018: 21 · 2017: 5
- FWCI
- 1.90
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Annual Review of Cancer Biology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Heart, Lung, and Blood Institute (T32HL076139)
- National Cancer Institute (R01CA123067)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cancer and biochemical research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
- Keywords
- reactive oxygen species, cancer, ROS signaling, oxidative stress, cancer cell death, hypoxia, antioxidant capacity, redox homeostasis, cell proliferation, cell survival
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