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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“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).”
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“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).”
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“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).”
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“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×
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Zhang, H., Wang, P., Zhang, J., Sun, Q., He, Q., He, X., Chen, H., & Ji, H. (2023) · Angewandte Chemie International Edition · doi:10.1002/anie.202316779 · Cited by 57
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Metabolic determinants of cellular fitness dependent on mitochondrial reactive oxygen species
Kong, H., Reczek, C. R., McElroy, G. S., Steinert, E. M., Wang, T., Sabatini, D. M., & Chandel, N. S. (2020) · Science Advances · doi:10.1126/sciadv.abb7272 · Cited by 56
“INTRODUCTION Reactive oxygen species (ROS) can activate signaling pathways that support cancer cell survival and proliferation as well as metastasis and drug resistance (1).”
Self-citationYang, R., Fu, S., Li, R., Zhang, L., Xu, Z., Cao, Y., Cui, H., Kang, Y., & Xue, P. (2020) · Theranostics · doi:10.7150/thno.50486 · Cited by 50
“Compared with normal cells, reactive oxygen species (ROS) are significantly upregulated in tumor cells due to increased metabolic rate, mitochondrial malfunction and enhanced activity of the peroxisome [1-4].”
BackgroundYouden, B., Jiang, R., Carrier, A. J., Servos, M. R., & Zhang, X. (2022) · ACS Nano · doi:10.1021/acsnano.2c06337 · Cited by 53
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NKX3.1 Localization to Mitochondria Suppresses Prostate Cancer Initiation
Papachristodoulou, A., Rodríguez-Calero, A., Panja, S., Margolskee, E. M., Virk, R. K., Milner, T. A., Martina, L. P., Kim, J. Y., Bernardo, M. D., Williams, A. B., et al. (2021) · Cancer Discovery · doi:10.1158/2159-8290.cd-20-1765 · Cited by 51
Boyenle, I. D., Oyedele, A.-Q. K., Ogunlana, A. T., Adeyemo, A. F., Oyelere, S. F., Akinola, O. B., Adelusi, T. I., Ehigie, L. O., & Ehigie, A. F. (2022) · Mitochondrion · doi:10.1016/j.mito.2022.01.006 · Cited by 50
Eom, S., Peak, J., Park, J., Ahn, S. H., Cho, Y. K., Jeong, Y., Lee, H.-S., Lee, J., Ignatova, E., Lee, S. E., et al. (2023) · Nature Cell Biology · doi:10.1038/s41556-023-01209-6 · Cited by 51
Tang, M., Dirks, K., Kim, S. Y., Qiu, Z., Gao, Y., Sun, D., Peruggia, G. A., Sallavanti, J., & Li, W. (2024) · Cell Death and Differentiation · doi:10.1038/s41418-024-01440-0 · Cited by 54
“This situation constitutes vulnerabilities that may be exploited for cancer therapy [14, 15].”
Diazaborines Are a Versatile Platform to Develop ROS‐Responsive Antibody Drug Conjugates**
António, J. P. M., Carvalho, J. I., André, A., et al. (2021) · Angewandte Chemie International Edition · doi:10.1002/anie.202109835 · Cited by 45
Metal ion chelation of poly(aspartic acid): From scale inhibition to therapeutic potentials
Adelnia, H., Sirous, F., Blakey, I., et al. (2022) · International Journal of Biological Macromolecules · doi:10.1016/j.ijbiomac.2022.12.256 · Cited by 44
Low-Dose Non-Targeted Effects and Mitochondrial Control
Averbeck, D. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms241411460 · Cited by 51
Recent Progress in Anti‐Tumor Nanodrugs Based on Tumor Microenvironment Redox Regulation
Yao, L., Zhu, X., Shan, Y., Zhang, L., Yao, J., & Xiong, H. (2024) · Small · doi:10.1002/smll.202310018 · Cited by 45
The molecular mechanisms of celecoxib in tumor development
Wen, B., Wei, Y., Mu, L.-L., Wen, G., & Zhao, K. (2020) · Medicine · doi:10.1097/md.0000000000022544 · Cited by 48
“level to ensure that the content of ROS does not exceed the threshold that the cancer cells can tolerate, and because of the high expression of ROS scavenging system, it shows a low level of ROS in cancer stem cells.([73,74]) Under the stimulation of hypoxia and hypoglycemia, the synthesis of mitochondrial ATP was sig…”
BackgroundSu, S.-H., Sundhar, N., Kuo, W., Lai, S., Kuo, C., Ho, T., Lin, P., Lin, S., Shih, C. Y., Lin, Y., et al. (2022) · Journal of Ethnopharmacology · doi:10.1016/j.jep.2022.115658 · Cited by 46
Gurhan, H., Bruzón, R. P., Kandala, S., Greenebaum, B., & Barnes, F. S. (2021) · Bioelectromagnetics · doi:10.1002/bem.22332 · Cited by 44
Islam, M. A., Medha, M. M., Nahar, A. U., Fahad, M. A. A., Siraj, M. A., & Seidel, V. (2023) · Nutrition and Cancer · doi:10.1080/01635581.2023.2183546 · Cited by 45
“The generation of ROS promotes anti-tumorigenic signaling and triggers oxidative stress–induced cancer cell death showing the dual characteristics of ROS (273).”
BackgroundThe conundrum of dietary antioxidants in cancer chemotherapy
Ilghami, R., Barzegari, A., Mashayekhi, M. R., Letourneur, D., Crépin, M., & Pavon‐Djavid, G. (2019) · Nutrition Reviews · doi:10.1093/nutrit/nuz027 · Cited by 41
Targeting fuel pocket of cancer cell metabolism: A focus on glutaminolysis
Sharma, S., Agnihotri, N., & Kumar, S. (2022) · Biochemical Pharmacology · doi:10.1016/j.bcp.2022.114943 · Cited by 42
Metabolic reprogramming: a bridge between aging and tumorigenesis
Drapela, S., Ilter, D., & Gomes, A. P. (2022) · Molecular Oncology · doi:10.1002/1878-0261.13261 · Cited by 41
Nrf2 Is a Potential Modulator for Orchestrating Iron Homeostasis and Redox Balance in Cancer Cells
Zhang, L., Zhang, J., Jin, Y., Yao, G., Zhao, H., Qiao, P., & Wu, S. (2021) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2021.728172 · Cited by 45
“Several mechanisms by which ROS production is enhanced in cancer cells have been described, such as oncogene activation, loss of cancer suppressors, and enhanced metabolism (Reczek and Chandel, 2017).”
BackgroundIbáñez, B., Melero, A., Montoro, A., Onofre, N. S., & Soriano, J. M. (2024) · Current Issues in Molecular Biology · doi:10.3390/cimb46110755 · Cited by 49
“Nevertheless, their high reactivity and mobility in the medium allow their action to propagate through it, potentially causing damage in locations far from their origin [38].”
Zhao, J., Wang, Z., Zhong, M., Xu, Q., Li, X., Chang, B., & Fang, J. (2021) · Journal of Medicinal Chemistry · doi:10.1021/acs.jmedchem.1c01362 · Cited by 43
NMT1 inhibition modulates breast cancer progression through stress-triggered JNK pathway
Deng, L., Gao, X., Liu, B., He, X., Xu, J., Qiang, J., Wu, Q., & Liu, S. (2018) · Cell Death and Disease · doi:10.1038/s41419-018-1201-x · Cited by 40
Cao, W., He, Y., Zhu, R., He, Y., Hao, Z., Zhao, Q., He, H., Wang, S., Li, C., & Gao, D. (2019) · Chemical Engineering Journal · doi:10.1016/j.cej.2019.122080 · Cited by 40
Ruiz, P. D., Hamilton, G. A., Park, J. W., & Gamble, M. J. (2019) · Molecular and Cellular Biology · doi:10.1128/mcb.00230-19 · Cited by 41
“leads to the formation of reactive oxygen species (ROS) that react with DNA and proteins (48).”
BackgroundTargeting the redox imbalance in mitochondria: A novel mode for cancer therapy
Mani, S., Swargiary, G., & Ralph, S. J. (2021) · Mitochondrion · doi:10.1016/j.mito.2021.11.002 · Cited by 43
Recent Progress of Surface Modified Nanomaterials for Scavenging Reactive Oxygen Species in Organism
Liu, J., Ma, L., Zhang, G., Chen, Y., & Wang, Z. (2021) · Bioconjugate Chemistry · doi:10.1021/acs.bioconjchem.1c00402 · Cited by 39
Zhang, Y., Lei, F., Qian, W., Zhang, C., Wang, Q., Liu, C., Ji, H., Liu, Z., & Wang, F. (2024) · Journal of Controlled Release · doi:10.1016/j.jconrel.2024.07.073 · Cited by 44
Pathophysiology of reactive oxygen species (ROS)
de la Lastra, J. M. P., Andrés, C. M. C., Munguira, E. B., Juan, C. A., & Pérez‐Lebeña, E. (2026) · Archives of Toxicology · doi:10.1007/s00204-025-04276-w · Cited by 61
“…rewire antioxidants—activating NRF2 and elevating GSH/thioredoxin systems—creating a narrow therapeutic window in which pushing ROS beyond buffering capacity triggers apoptosis or ferroptosis, whereas indiscriminate scavenging blunts therapy and fosters resistance (Reczek and Chandel 2017).”
Sui, Y., Gu, Y., Lu, Y., Yu, C., Zheng, J., & Qi, H. (2021) · Marine Drugs · doi:10.3390/md19020092 · Cited by 39
“However, the increase in ROS at high concentrations can enhance the anti-tumor signals and trigger the apoptosis of cancer cells induced by oxidative stress, so that ROS exhibit anti-cancer effects in cancer cells [35].”
BackgroundTumor Immune Evasion Induced by Dysregulation of Erythroid Progenitor Cells Development
Grzywa, T. M., Justyniarska, M., Nowis, D., & Gołąb, J. (2021) · Cancers · doi:10.3390/cancers13040870 · Cited by 41
“Therefore, current studies focus on increasing rather than decreasing ROS levels in TME due to increased vulnerability to oxidative stress-induced apoptosis [241].”
BackgroundMitochondrial Redox Metabolism: The Epicenter of Metabolism during Cancer Progression
Choudhury, F. K. (2021) · Antioxidants · doi:10.3390/antiox10111838 · Cited by 44
Metabolic Adaptation-Mediated Cancer Survival and Progression in Oxidative Stress
Tang, Y., Zhang, Z., Chen, Y., Qin, S., Zhou, L., Gao, W., & Shen, Z. (2022) · Antioxidants · doi:10.3390/antiox11071324 · Cited by 47
The action and resistance mechanisms of Lenvatinib in liver cancer
Buttell, A., & Qiu, W. (2023) · Molecular Carcinogenesis · doi:10.1002/mc.23625 · Cited by 38
“33 Connecting ROS back to this study, ROS elevation increases EGFR autophosphorylation.”
BackgroundZayed, N., Aly, H. F., El‐mezayen, H. A., & El-Salamony, H. E. (2019) · Toxicology Reports · doi:10.1016/j.toxrep.2019.08.007 · Cited by 37
“It was proven that ROS are a direct cause of somatic cell mutagenesis and they are cancer promoter [67], so they are considered as life threatening and oncogenes product.”
BackgroundCortez-Trejo, M. C., Olivas-Aguirre, F. J., Dufoo‐Hurtado, E., Castañeda, R., Villegas-Quintero, H., Medina‐Franco, J. L., Mendoza, S., & Wall‐Medrano, A. (2022) · Biomolecules · doi:10.3390/biom12111649 · Cited by 39
“ROS plays a dual role in cancer by promoting cell proliferation–survival–adaptation to hypoxia and by triggering oxidative-stress cancer cell death, both cases handled with ROS-manipulation therapies [51].”
BackgroundOlcha, P., Winiarska‐Mieczan, A., Kwiecień, M., Nowakowski, Ł., Miturski, A., Semczuk, A., Kiczorowska, B., & Gałczyński, K. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23126703 · Cited by 38
“ROS are among the factors responsible for inducing the neoplastic transformation of cells and play a two-fold role in neoplasia: on the one hand, they can promote pro-tumorigenic signalling, facilitating the proliferation of tumour cells, their survival and adaptation to hypoxia, and on the other, they can promote ant…”
BackgroundBarra, J., Crosbourne, I., Roberge, C. L., Ramos, R. B., Warren, J., Matteson, K., Wang, L., Jourd’heuil, F. L., Borisov, S. M., Bresnahan, E. R., et al. (2024) · Oncogene · doi:10.1038/s41388-023-02933-x · Cited by 48
“In non-cancerous cells, ROS increase is harmful but in cancer cells, iron increase and subsequent ROS overproduction can enhance their invasive and metastatic capacity by inducing loss of matrix attachment, promoting tumor angiogenesis, and increasing DNA damage [4].”
The Redox Paradox: Cancer’s Double-Edged Sword for Malignancy and Therapy
Ranbhise, J. S., Singh, M. K., Ju, S., Han, S., Yun, H. R., Kim, S. S., & Kang, I. (2025) · Antioxidants · doi:10.3390/antiox14101187 · Cited by 47
“The O 2 •− is short-lived, local, and does not cross the cellular membrane easily, generated from mitochondrial complexes 1, 2, and 3 [17,18].”
Ralph, S. J., Nozuhur, S., ALHulais, R. A., Rodríguez‐Enríquez, S., & Moreno‐Sánchez, R. (2019) · Medicinal Research Reviews · doi:10.1002/med.21589 · Cited by 37
“ROS production systems become elevated in more advanced stage cancer cells to promote their growth and survival.(33,77,78) The tumor microenvironment during rapacious growth phases will concomitantly cause intermittent periods of hypoxia, acidosis,(82,83) and nutrient deprivation resulting in hypoglycemia, all factors…”
BackgroundTea and Its Components Prevent Cancer: A Review of the Redox-Related Mechanism
Mao, X., Xiao, X., Chen, D., Yu, B., & He, J. (2019) · International Journal of Molecular Sciences · doi:10.3390/ijms20215249 · Cited by 38
“Enzymatic antioxidants mainly consist of superoxide dismutases (SODs), peroxiredoxins (PRXs), glutathione peroxidases (GPXs), and catalase (CAT) [26,27].”
BackgroundFrom Fluorescent Probes to the Theranostics Platform
Wei, P., Wang, Q., & Yi, T. (2022) · Chinese Journal of Chemistry · doi:10.1002/cjoc.202200122 · Cited by 38
Radjenovic, P. M., & Hardwick, L. J. (2019) · Physical Chemistry Chemical Physics · doi:10.1039/c8cp04652b · Cited by 36
Oh, S., Choi, S.-Y., Choi, H., Ryu, H., Kim, Y.-J., Jung, H., Cho, J., Kim, C., Park, S.-H., Kwon, T., et al. (2019) · The FASEB Journal · doi:10.1096/fj.201802415rr · Cited by 36
“On the contrary, ROS also could induce oxidative stress–mediated cancer cell death (32).”
BackgroundMacLean, L., Karcz, D., Jenkins, H., McClean, S., Devereux, M. M., Howe, O. L., Pereira, M. D., May, N. V., Enyedy, É. A., & Creaven, B. S. (2019) · Journal of Inorganic Biochemistry · doi:10.1016/j.jinorgbio.2019.110702 · Cited by 38
Fisetin, a phytopolyphenol, targets apoptotic and necroptotic cell death in HepG2 cells
Sundarraj, K., Raghunath, A., Panneerselvam, L., & Perumal, E. (2019) · BioFactors · doi:10.1002/biof.1577 · Cited by 36
Schuster, C., Wolpert, N., Moustaïd‐Moussa, N., & Gollahon, L. (2022) · Antioxidants · doi:10.3390/antiox11030591 · Cited by 36
Wang, Y., Noman, A., Zhang, C., AL‐Bukhaiti, W. Q., & Abed, S. M. (2024) · Frontiers in Marine Science · doi:10.3389/fmars.2024.1500870 · Cited by 48
The influence of mitochondrial-directed regulation of Wnt signaling on tumorigenesis
Delgado‐Deida, Y., Alula, K. M., & Theiss, A. L. (2020) · Gastroenterology report · doi:10.1093/gastro/goaa025 · Cited by 34
Lahiri, T., Brambilla, L., Andrade, J., Askenazi, M., Ueberheide, B. M., & Levy, D. E. (2021) · Molecular Oncology · doi:10.1002/1878-0261.12928 · Cited by 37
Chen, P., Sharma, A., Weiher, H., & Schmidt‐Wolf, I. G. H. (2024) · Journal of Experimental & Clinical Cancer Research · doi:10.1186/s13046-024-02990-4 · Cited by 41
“Though, tumor cells possess a more potent antioxidant capacity than T cells [53, 118].”
BackgroundSastre‐Serra, J., Ahmiane, Y., Roca, P., Oliver, J., & Pons, D. G. (2018) · International Journal of Food Sciences and Nutrition · doi:10.1080/09637486.2018.1540558 · Cited by 33
“…overproduction of ROS, or a suppression of cell capacity to remove ROS, results in a significant increase in intracellular ROS, causing cell damage (oxidation of lipids, proteins and DNA) and ultimately causing cell death (Trachootham et al. 2009; Panieri and Santoro 2016; Reczek and Chandel 2017).”
BackgroundJayathilake, A. G., Kadife, E., Luwor, R. B., Nurgali, K., & Su, X. Q. (2019) · Nutrition & Metabolism · doi:10.1186/s12986-019-0382-3 · Cited by 36
Kaga, Y., Kuda, T., Taniguchi, M., Yamaguchi, Y., Takenaka, H., Takahashi, H., & Kimura, B. (2020) · LWT · doi:10.1016/j.lwt.2020.110029 · Cited by 35
Giacosa, S., Pillet, C., Séraudie, I., Guyon, L., Wallez, Y., Roelants, C., Battail, C., Evrard, B., Chalmel, F., Barette, C., et al. (2021) · Cancers · doi:10.3390/cancers13030576 · Cited by 43
“Therefore, an emerging view is that such vulnerability can be exploited to selectively kill cancer cells [77].”
BackgroundRamundo, V., Giribaldi, G., & Aldieri, E. (2021) · Cancers · doi:10.3390/cancers13123093 · Cited by 37
“ROS have a dual role in cancer: high levels of ROS are cytotoxic but they are also pro-tumorigenic [25], as the hyperproliferation of cancer cells is accompanied by a high production of ROS; however, in this way, cancer cells are able to adapt themselves to thrive in conditions that can counteract this oxidative stres…”
BackgroundMcGarry, D. J., Armstrong, G., Castino, G. F., Mason, S. M., Clark, W. A., Shaw, R., McGarry, L., Blyth, K., & Olson, M. F. (2021) · Cancer Letters · doi:10.1016/j.canlet.2021.07.039 · Cited by 35
“ROS have been found elevated in many cancer types and can activate several signal transduction pathways that promote cellular growth and proliferation [13] [14].”
Xu, Y., Wang, C., Sui, L., et al. (2023) · Journal of Materials Chemistry C · doi:10.1039/d2tc04897c · Cited by 34
Metabolic Reprogramming: A Friend or Foe to Cancer Therapy?
McCann, C. K., & Kerr, E. M. (2021) · Cancers · doi:10.3390/cancers13133351 · Cited by 36
“Reactive Oxygen Species (ROS) generated as a by-product of mitochondrial metabolism were originally considered cytotoxic, but demonstrably can regulate cell growth and adaption to cellular stress [22].”
BackgroundStimuli-responsive (nano)architectures for phytochemical delivery in cancer therapy
Zandieh, M. A., Farahani, M. H., Daryab, M., Motahari, A., Gholami, S., Salmani, F., Karimi, F., Samaei, S. S., Rezaee, A., Rahmanian, P., et al. (2023) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2023.115283 · Cited by 35
Oxidative Stress and Inflammation Can Fuel Cancer
Vaidya, F. U., Chhipa, A. S., Sagar, N., & Pathak, C. (2020) · Springer eBooks · doi:10.1007/978-981-15-1568-2_14 · Cited by 37
ROS-Mediated Anti-Angiogenic Activity of Cerium Oxide Nanoparticles in Melanoma Cells
Yong, J. M., Fu, L., Tang, F., Yu, P., Kuchel, R. P., Whitelock, J. M., & Lord, M. S. (2022) · ACS Biomaterials Science & Engineering · doi:10.1021/acsbiomaterials.1c01268 · Cited by 33
Vonnie, J. M., Rovina, K., Mariah, A. M. A., Erna, K. H., Felicia, W. X. L., & Aqilah, M. N. N. (2022) · International Journal of Environmental Science and Technology · doi:10.1007/s13762-022-04487-z · Cited by 35
Sulfur-based fluorescent probes for biological analysis: A review
Hu, G., Xu, H.-D., & Fang, J. (2024) · Talanta · doi:10.1016/j.talanta.2024.126515 · Cited by 32
The Yin and Yang of cancer genes
Bashyam, M. D., Animireddy, S., Bala, P., Naz, A., & George, S. A. (2019) · Gene · doi:10.1016/j.gene.2019.04.025 · Cited by 31
Synergistic Antioxidant Activity of Size Controllable chitosan-templated Prussian Blue Nanoparticle
Oh, H., Lee, J. S., Sung, D., et al. (2019) · Nanomedicine · doi:10.2217/nnm-2019-0223 · Cited by 32
Counteracting Action of Curcumin on High Glucose-Induced Chemoresistance in Hepatic Carcinoma Cells
Soni, V. K., Mehta, A., Ratre, Y. K., et al. (2021) · Frontiers in Oncology · doi:10.3389/fonc.2021.738961 · Cited by 31
“ROS has a dual role to play in cancer biology; and its low level upkeeps the survival of cancer stem cells, which correlates with chemoresistance (44, 45).”
BackgroundJia, Y., Wu, C., Rivera‐Piza, A., Kim, Y., Lee, J. H., & Lee, S. (2022) · Antioxidants · doi:10.3390/antiox11040749 · Cited by 33
“Reactive oxygen species (ROS) have a dual role in cancer [2].”
BackgroundLiu, S., Dong, L., Shi, W., Zheng, Z., Liu, Z., Meng, L., Xin, Y., & Jiang, X. M. (2022) · Frontiers in Pharmacology · doi:10.3389/fphar.2022.921070 · Cited by 31
“High levels of ROS-damaged proteins, lipids, and deoxyribonucleic acid (DNA) promote clonal expansion and tumor growth by protecting initial cells from oxidative toxicity and apoptosis (Reczek and Chandel, 2017).”
BackgroundStructural insights into the activation of ataxia-telangiectasia mutated by oxidative stress
Howes, A. C., Perišić, O., & Williams, R. L. (2023) · Science Advances · doi:10.1126/sciadv.adi8291 · Cited by 34
“Quantification of the Coomassie-stained Phos-tag gel bands to determine % p53(1-102) substrate phosphorylation using data from three biological replicates (right).”
BackgroundMethodInfluentialMutungi, M. M., Muema, F. W., Kimutai, F., Xu, Y., Zhang, H., Chen, G., & Guo, M. (2021) · Pharmaceuticals · doi:10.3390/ph14030266 · Cited by 30
“The effective regulation of ROS via an antioxidant system could reduce cancer manifestation and also help in cancer treatment [38].”
BackgroundSensing Reactive Oxygen Species with Photoacoustic Imaging Using Conjugation-Extended BODIPYs
Merkes, J. M., Hasenbach, A., Kiessling, F. M., Hermann, S., & Banala, S. (2021) · ACS Sensors · doi:10.1021/acssensors.1c01674 · Cited by 30
Targeting Glioblastoma via Selective Alteration of Mitochondrial Redox State
Sumiyoshi, A., Shibata, S., Zhelev, Z., Miller, T. J., Lazarova, D., Aoki, I., Obata, T., Higashi, T., & Bakalova, R. (2022) · Cancers · doi:10.3390/cancers14030485 · Cited by 28
Moccia, F. D., & Montagna, D. (2023) · Cells · doi:10.3390/cells12091261 · Cited by 31
“The rate of basal ROS production in cancer cells is enhanced by multiple mechanisms [2,9], such as metabolic disturbances, adaptation to hypoxia, oncogene activation, and loss of tumor suppressors.”
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“On the other hand, its increase can promote antitumor properties and trigger the death of cancer cells induced by oxidative stress (Reczek and Chandel 2017; Wang et al. 2021).”
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Background
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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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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