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).”
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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“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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Balakrishnan, V., Sindhu, G., Vinothkumar, V., Ramachandhiran, D., Jawaharlal, S., & Vennila, L. (2022) · Journal of Food Biochemistry · doi:10.1111/jfbc.14465 · Cited by 11
The Biocatalysis in Cancer Therapy
Liu, J., Ren, H., Tang, T., Wang, J., Fang, J., Huang, C., Zheng, Z., & Qin, B. Y. (2023) · ACS Catalysis · doi:10.1021/acscatal.3c01363 · Cited by 12
Mechanistic Development of Cancers Associated with Processed Meat Products: A Review
Bedale, W. A., Milkowski, A. L., Czuprynski, C. J., & Richards, M. P. (2023) · Meat and Muscle Biology · doi:10.22175/mmb.15762 · Cited by 11
Enzyme-free hydrogen peroxide sensing based on heterogeneous SnO2@CuO/CF via interfacial engineering
Zou, G., Sun, L., Huo, L.-H., et al. (2024) · Electrochimica Acta · doi:10.1016/j.electacta.2024.144163 · Cited by 11
NRF2-driven redox metabolism takes center stage in cancer metabolism from an outside-in perspective
Choi, E.-J., & Jeon, S. (2020) · Archives of Pharmacal Research · doi:10.1007/s12272-020-01224-3 · Cited by 10
Hong, S. H., Koo, M., Lee, M. H., Seon, G. M., Park, Y. J., Jeong, H., Kim, D., & Park, J. (2021) · Regenerative Biomaterials · doi:10.1093/rb/rbab005 · Cited by 11
Pal, S., Singh, N., Dev, I., et al. (2021) · Toxicology and Applied Pharmacology · doi:10.1016/j.taap.2021.115819 · Cited by 11
Synthesis of Lasalocid-Based Bioconjugates and Evaluation of Their Anticancer Activity
Antoszczak, M., Otto-Ślusarczyk, D., Kordylas, M., et al. (2022) · ACS Omega · doi:10.1021/acsomega.1c05434 · Cited by 11
“56,57 In our study, we observed a signi fi cantly higher level of ROS in cancer cells compared to that in normal cells after treatment with LAS bioconjugate with gemcitabine (compound 12 ) (Figures 5A and6A).”
Polloni, L., Costa, T. R., Morais, L. P., Borges, B. C., Teixeira, S. C., Fernandes, T. A. D. M., Correia, L. I. V., Bastos, L. M., Amorim, F. G., Quinton, L., et al. (2023) · Cellular Signalling · doi:10.1016/j.cellsig.2023.110785 · Cited by 11
Bose, G. S., Jindal, S., Landage, K. B., Jindal, A., Mahale, M. P., Kulkarni, A. P., & Mittal, S. P. K. (2024) · FEBS Journal · doi:10.1111/febs.17253 · Cited by 10
Stinson, J. A., Sheen, A. M., Lax, B. M., Yang, G. N., Duhamel, L., Santollani, L., Fink, E., Palmeri, J. R., & Wittrup, K. D. (2024) · Molecular Cancer Therapeutics · doi:10.1158/1535-7163.mct-24-0163 · Cited by 11
Laatsch, B. F., Ali, B. A., Berthiaume, A. R., Cunningham, G. C., Duncan, S. M., Hau, N., Ho, A., Loomis, M. A., Lowater, H. R., McNally, B. L., et al. (2024) · Indian Journal of Clinical Biochemistry · doi:10.1007/s12291-024-01284-y · Cited by 10
“To avoid this, cancer cells increase antioxidants to keep RONS at a level conducive to tumor growth [ 29].”
Zamyatina, E. A., Goryacheva, O. A., Popov, A. L., & Popova, N. R. (2024) · Antioxidants · doi:10.3390/antiox13121445 · Cited by 10
Cuproptosis: an emerging domain for copper-based nanomaterials mediated cancer therapy
Zhao, F., Zhao, Z., Gao, H., Zhang, Y., Qi, J., Yu, H., Wang, C., Xu, J., Yousaf, M. Z., Che, S., et al. (2024) · MedMat. · doi:10.1097/mm9.0000000000000010 · Cited by 11
Eng, Z. H., Aziz, A. A., Ng, K. L., & Junit, S. M. (2023) · Frontiers in Molecular Biosciences · doi:10.3389/fmolb.2023.1237548 · Cited by 12
“Reactive oxygen species (ROS) is a group of oxygen-containing molecules produced as by-products of cellular metabolic processes (Reczek and Chandel, 2017).”
BackgroundA new biocompatible silver/polypyrrole composite with in vitro antitumor activity
Lima, E. M. D. A., Holanda, V. N., Ratkovski, G. P., da Silva, W. V., do Nascimento, P. H., de Figueiredo, R. C. B. Q., & de Melo, C. P. (2021) · Materials Science and Engineering C · doi:10.1016/j.msec.2021.112314 · Cited by 9
Rasheed, H. M., Wahid, F., Ikram, M., Qaisar, M., Shah, A. J., & Khan, T. (2021) · Tropical Journal of Pharmaceutical Research · doi:10.4314/tjpr.v20i9.21 · Cited by 10
“Thus, cancer cells are more prone to apoptosis as compared to normal cells when treated with ROS inducing compounds [29].”
BackgroundSex differences in gene regulatory networks during mid-gestational brain development
de Toledo, V. H. C., Feltrin, A. S., Barbosa, A. D. L., Tahira, A. C., & Brentani, H. (2022) · Frontiers in Human Neuroscience · doi:10.3389/fnhum.2022.955607 · Cited by 14
“These intricate interactions are signaling factors for proliferation, differentiation, apoptosis, and autophagy when ROS is overabundant (Reczek and Chandel, 2017).”
BackgroundA guide to reactive oxygen species in tumour hypoxia: measurement and therapeutic implications
Hacker, L., Sarsam, E., Conway, S. J., & Hammond, E. M. (2025) · Molecular Oncology · doi:10.1002/1878-0261.70151 · Cited by 13
“These modifications enable ROS to function as signalling molecules that influence cellular activities, which have been reviewed extensively [10,21,26,27], and are therefore not the primary focus here.”
Exploring How Reactive Oxygen Species Contribute to Cancer via Oxidative Stress
Tavakolpournegari, A., Moosavi, S. S., Matinahmadi, A., Zayani, Z., & Bidooki, S. H. (2025) · Stresses · doi:10.3390/stresses5040069 · Cited by 10
“Oncogenic KRAS mutations support low intracellular ROS by activating antioxidant gene programs and reshaping metabolic pathways [180] while the hypoxic tumor microenvironment drives chronic ROS accumulation through mitochondrial and glycolytic rewiring and enhanced antioxidant responses [2].”
InfluentialMoghadam, D., Zarei, R., Rostami, A., Samare‐Najaf, M., Ghojoghi, R., Savardashtaki, A., Jafarinia, M., Vakili, S., & Irajie, C. (2024) · Anti-Cancer Agents in Medicinal Chemistry · doi:10.2174/0118715206317999240708062744 · Cited by 9
de Sousa, V. M., Duarte, S. S., Ferreira, R. C., de Sousa, N. F., Scotti, M. T., Scotti, L., da Silva, M. S., Tavares, J. F., de Moura, R. O., Gonçalves, J. C. R., et al. (2024) · Molecules · doi:10.3390/molecules29225344 · Cited by 9
Mechanism analysis and targeted therapy of IDH gene mutation in glioma
Ma, X. (2025) · American Journal of Cancer Research · doi:10.62347/nsxc2205 · Cited by 10
Verma, M., Fatima, S., Syed, A., et al. (2025) · Naunyn-Schmiedeberg s Archives of Pharmacology · doi:10.1007/s00210-025-03899-1 · Cited by 9
“ROS have been found to have a much greater baseline level in cancer cells in comparison to healthy cells (Sena and Chandel 2012; Reczek and Chandel 2017; Hasan et al. 2022).”
Mostafa, N., Salem, A. M. H., Mansour, S. Z., El-Sonbaty, S. M., Moawed, F. S., & Kandil, E. (2022) · Technology in Cancer Research & Treatment · doi:10.1177/15330338221085376 · Cited by 9
“In essence, there are 2 faces of ROS in cancer, pro-and anti-tumorigenic.(108) Accumulating evidence has demonstrated that DEN exposure has been associated with hepatocellular accumulation of ROS resulting in DNA oxidative damage, a mechanism that may further enhance DEN-induced hepatocarcinogenesis.”
BackgroundPeroxiredoxin 5 is involved in cancer cell invasion and tumor growth of oral squamous cell carcinoma
Lee, M. K., Zhang, X., Kim, H. J., & Hwang, Y. S. (2021) · Oral Diseases · doi:10.1111/odi.13910 · Cited by 9
Kyriakou, S., Tragkola, V., Plioukas, M., Anestopoulos, I., Chatzopoulou, P. S., Sarrou, E., Trafalis, D. T., Deligiorgi, M. V., Franco, R., Pappa, A., et al. (2021) · Plants · doi:10.3390/plants10112472 · Cited by 10
Demircan, M. B., Mgbecheta, P. C., Kresinsky, A., Schnoeder, T. M., Schröder, K., Heidel, F. H., & Böhmer, F. (2022) · Antioxidants · doi:10.3390/antiox11030513 · Cited by 10
Quantitative estimation of intracellular oxidative stress in human tissues
Bai, J., Tan, R., An, Z., & Xu, Y. (2022) · Briefings in Bioinformatics · doi:10.1093/bib/bbac206 · Cited by 9
“Under stressful conditions of any kind, oxidizing molecules such as reactive oxygen [3, 4] or/and nitrogen [5, 6] species will be produced intracellularly and/or by local immune cells.”
Modulation of reactive oxygen species in cancers: recent advances
Ganesh, J. M., Prerana, P., Dharmarajan, A., Warrier, S. R., & Gandhirajan, R. K. (2022) · Free Radical Research · doi:10.1080/10715762.2022.2133704 · Cited by 12
Drzał, A., Delalande, A., Dziurman, G., Pichon, C., Swakoń, J., & Elas, M. (2023) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2023.02.022 · Cited by 9
“Furthermore, cellular responses to ROS depend on their type, location, and concentration [52].”
Development of chromone-thiazolidine-2,4-dione Knoevenagel conjugates as apoptosis inducing agents
Galla, M. S., Kale, N. B., Sharma, A., et al. (2024) · Bioorganic & Medicinal Chemistry Letters · doi:10.1016/j.bmcl.2024.129853 · Cited by 8
Zhu, J., Long, Y., He, Y., Liu, S., Wu, X., Teng, K., Liu, W., Feng, F., & Qu, W. (2025) · Journal of Medicinal Chemistry · doi:10.1021/acs.jmedchem.5c01521 · Cited by 8
C-13 Hyperpolarized MR Spectroscopy for Metabolic Imaging of Brain Tumors
Viswanath, P., Li, Y., & Ronen, S. M. (2019) · Springer eBooks · doi:10.1007/978-3-030-27359-0_12 · Cited by 8
Ferraz, A. P. C. R., Sussulini, A., Garcia, J., Costa, M. R., Francisqueti-Ferron, F., Ferron, A. J. T., Silva, C. D. A., Corrente, J., Manfio, V., Namba, V., et al. (2020) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2020/7240216 · Cited by 8
“These species play a role in various fields of biology and medicine of cancer on protumorigenic signaling, cell proliferation, and tumorigenesis and transcription factor activation, which in turn can promote cytokines and chemokines such as IL-6 production in inflammation pathways as well as regulating and inducing ap…”
BackgroundKumbhakonam, S., Saroj, S., Venkatesan, N., et al. (2020) · Bioorganic & Medicinal Chemistry Letters · doi:10.1016/j.bmcl.2020.127594 · Cited by 8
Brown, S. R., Bates, J. C., Avera, A. D., & Kim, Y. (2021) · Cells Tissues Organs · doi:10.1159/000516574 · Cited by 8
“Contrarily, ROS generation can induce apoptosis or autophagy [Dan Dunn et al., 2015; Reczek and Chandel, 2017].”
BackgroundVu, M., Kassouf, N., & Appiah, S. S. (2021) · Antioxidants · doi:10.3390/antiox10091456 · Cited by 8
“ROS are by-products of normal cellular metabolism and in small amounts are necessary for maintaining cellular homeostasis [56].”
BackgroundPolymorphonuclear Neutrophils and Tumors: Friend or Foe?
Szulc-Kiełbik, I., & Klink, M. (2022) · Experientia supplementum · doi:10.1007/978-3-030-91311-3_5 · Cited by 9
When starvation therapy meets chemodynamic therapy
Blum, N. T., Fu, L., Lin, J., & Huang, P. (2022) · ChemPhysMater · doi:10.1016/j.chphma.2022.05.001 · Cited by 8
Combination strategies to target metabolic flexibility in cancer
Krstić, J., Schindlmaier, K., & Prokesch, A. (2022) · International review of cytology · doi:10.1016/bs.ircmb.2022.03.001 · Cited by 9
Roy, S., Mitra, P., Acharya, S., Roy, S. S., Ghosh, S., Maji, M., Modak, N., Ghosh, N., Acharya, M., Singh, S., et al. (2022) · Inorganic Chemistry Frontiers · doi:10.1039/d2qi01079h · Cited by 8
Fragoulis, A., Tohidnezhad, M., Kubo, Y., Wruck, C. J., Craveiro, R. B., Bock, A., Wolf, M. F., Pufe, T., Jahr, H., & Suhr, F. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms24097722 · Cited by 10
“On the one hand, they foster protumorigenic signaling, hence, cancer cell proliferation; on the other hand, they provide antitumorigenic signaling that results in oxidative stress-induced cancer cell death [45].”
BackgroundBoungou-Tsona, G., Gainche, M., Decombat, C., Ripoche, I., Bikindou, K., Delort, L., Caldefie‐Chezet, F., Loumouamou, A. N., & Chalard, P. (2023) · Plants · doi:10.3390/plants12020386 · Cited by 8
Dubey, A., & Sharma, B. (2025) · Drugs and Drug Candidates · doi:10.3390/ddc4020023 · Cited by 7
“The final progression stage is involved in the conversion of benign lesions into cancerous lesions, causing metastasis [31–34].”
Tamir, T. Y., Chaudhary, S., Li, A. X., Trojan, S., Flower, C. T., Vo, P., Cui, Y., Davis, J. C., Mukkamala, R. S., Venditti, F. N., et al. (2024) · Molecular Cell · doi:10.1016/j.molcel.2025.05.007 · Cited by 8
Targeting Oxidative Stress in Carcinogenesis: Oleanolic Acid and Its Molecular Pathways
Günther, A., Kulawik, M., Sip, S., Zalewski, P., Jarmołowska‐Jurczyszyn, D., Stawicki, P., & Barbara, B.-C. (2026) · Antioxidants · doi:10.3390/antiox15010067 · Cited by 9
“However, prolonged exposure to conditions that promote oxidative stress—such as chronic inflammation, metabolic disorders, xenobiotic exposure or ionizing radiation—leads to excessive ROS production and accumulation of DNA damage [75,76].”
pan, B., Kang, J.-L., Zheng, R., Wei, C., & Zhi, Y. (2024) · Pathology - Research and Practice · doi:10.1016/j.prp.2024.155324 · Cited by 8
The role of reactive oxygen species in screening anticancer agents
Zhang, S., Xu, X., Dang, Z., Sun, T., & Zhang, H. (2018) · Cancer translational medicine · doi:10.4103/ctm.ctm_6_18 · Cited by 7
Sur, D. G., Gorzo, A., Sabarimurugan, S., Krishnan, S. M., Lungulescu, C. V., Volovăț, S. R., & Burz, C. C. (2021) · Anti-Cancer Agents in Medicinal Chemistry · doi:10.2174/1871520621666210901100827 · Cited by 8
Gupta, P., Singh, A., Verma, A. K., et al. (2022) · Indian Journal of Clinical Biochemistry · doi:10.1007/s12291-022-01055-7 · Cited by 7
“Increased ROS may have negative consequences for essential macromolecules including proteins, ribonucleic acids (DNA and RNA), and lipids, ultimately leading to cell death [33].”
BackgroundPeshkov, A. A., Urazaliyeva, A., Saiduldinova, D., Kulbergenov, K., Alhassan, N. B., Beisenbayev, A. R., Shabdan, Y., Umbayev, B. A., Peshkov, V. A., Atabaev, T. S., et al. (2025) · International Journal of Molecular Sciences · doi:10.3390/ijms26073304 · Cited by 6
“…However, when produced in excess, ROS are implicated in a range of inflammatory conditions, including diabetes [2], neurodegenerative disorders [3], ischemia–reperfusion injury [4], impaired stem cell re-newal [5], and cancer [6]. injury [4], impaired stem cell renewal [5], and cancer [6].”
Recent advances in redox-responsive polysaccharide-based nanostructures for cancer therapy
Li, J., Wang, J., Huang, Y., Liu, Y., Xiao, H., & Seidi, F. (2026) · Carbohydrate Polymers · doi:10.1016/j.carbpol.2026.124969 · Cited by 8
Exploiting lipotoxicity for the treatment of liver cancer
Rudalska, R., Zender, L., & Dauch, D. (2021) · British Journal of Cancer · doi:10.1038/s41416-021-01479-7 · Cited by 7
Silencing superoxide dismutases (SOD1&SOD2) potentiates ROS-induced apoptosis in chordoma cells
Seven, D., Tecimel, D., Özbey, U., Kızılilsoley, N., Nıkerel, E., Dalan, A. B., Türe, U., & Bayrak, Ö. F. (2025) · Molecular Biology Reports · doi:10.1007/s11033-025-10239-2 · Cited by 6
“The fundamental role of ROS in carcinogenesis to hyperactivate protumorigenic signaling events as well as contributing to hallmarks of cancer by inducing DNA damage, gene expression and function is well established [4, 5].”
Retinoids and Reactive Oxygen Species in Cancer Cell Death and Therapeutics
El‐Baba, C., Eid, A. H., Shaito, A., Kobeissy, F. H., & Darwiche, N. (2021) · Springer eBooks · doi:10.1007/978-981-15-4501-6_186-1 · Cited by 6
Redox regulation of hybrid metabolic state in breast cancer metastasis
Attri, K. S., Park, J. H., & Kaipparettu, B. A. (2022) · Annals of Translational Medicine · doi:10.21037/atm-22-3730 · Cited by 5
“While low levels of ROS activate oncogenic signaling by redox mechanisms, high levels of ROS referred to as oxidative stress damages DNA, protein, and lipids (1).”
BackgroundŠeremet, D., Durgo, K., Kosanović, J., Huđek, A., Mandura, A., Cebin, A. V., & Komes, D. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms242316975 · Cited by 7
“…increased concentrations of ROS compared with normal cells but are more sensitive to disturbances in the redox balance, which can activate various signaling pathways leading to cell death [25]. disturbances in the redox balance, which can activate various signaling pathways leading cell death [25].”
BackgroundOgbodo, A. K., Mustafov, D., Arora, M., Lambrou, G. Ι., Braoudaki, M., & Siddiqui, S. S. (2024) · Heliyon · doi:10.1016/j.heliyon.2024.e24286 · Cited by 6
“Similarly, ROS have being described to be a cornerstone in events leading to diseases of protracted duration, such as cancer [62].”
BackgroundThe Dual Role of Oxidative Stress in Lung Cancer
Ahmed, A. M. (2019) · Springer eBooks · doi:10.1007/978-981-13-8413-4_5 · Cited by 7
de Abreu, J. S. S., & Fernandes, J. (2021) · Molecular Biology Reports · doi:10.1007/s11033-021-06524-5 · Cited by 6
Cai, P., Sheng, G., Jiang, S., et al. (2022) · Frontiers in Pharmacology · doi:10.3389/fphar.2022.837055 · Cited by 6
“CAT, a heme protein mainly in the peroxisomes of most cells, converts H2O2 into H2O and O2 in the absence of any cofactors (Reczek and Chandel, 2017).”
BackgroundMohammed, M. R. S., Alzahrani, F. A., Hosawi, S. B. I., Choudhry, H., & Khan, M. I. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23126653 · Cited by 6
“References [12,13] showed that disproportionate ROS is harmful to cells, resulting in oxidative damage to RNA, DNA, and proteins.”
BackgroundHarnessing Redox Disruption to Treat Human Herpesvirus 8 (HHV-8) Related Malignancies
Gothland, A., Jary, A., Grange, P., Leducq, V., Remigereau, L. B., Dupin, N., Marcelin, A., & Cálvez, V. (2022) · Antioxidants · doi:10.3390/antiox12010084 · Cited by 6
“Compared to normal cells, cancer cells produce more spatially confined mitochondria- and NOX-dependent ROS [26,27].”
BackgroundTumor-associated redox state in metastatic colorectal cancer
Бурлака, А. П., Ganusevich, І. І., Burlaka, A. A., et al. (2019) · Experimental Oncology · doi:10.32471/exp-oncology.2312-8852.vol-41-no-2.13128 · Cited by 6
Understanding the Dual Role of Macrophages in Tumor Growth and Therapy: A Mechanistic Review
Summer, M., Riaz, S., Ali, S., Noor, Q., Ashraf, R., & Khan, R. R. M. (2025) · Chemistry & Biodiversity · doi:10.1002/cbdv.202402976 · Cited by 8
“It has been demonstrated that ROS could also stimulate nuclear translocation of NF-κ B which is a transcription factor that is involved in growth, differentiation, and survival of cell to induce tumorigenesis and metastasisbyregulatingdifferentgenes[125].”
Lalmuansangi, C., Lalfakawmi, Nghakliana, F., et al. (2025) · Discover Oncology · doi:10.1007/s12672-025-02138-6 · Cited by 5
“The development and progression of many diseases, including cancer, is associated with elevated levels of intracellular reactive oxygen species (ROS), which can occur due to either increased ROS production or a weakened antioxidant defense system [47–49].”
Zeng, Y., Lu, X., Wang, Y.-D., He, J., Cao, H., Zhang, L., & Cheng, L. (2025) · Frontiers in Oncology · doi:10.3389/fonc.2025.1586515 · Cited by 7
“In contrast, normal cells maintain redox homeostasis through a sophisticated antioxidant system, which is critical for preventing oxidative damage (19, 20).”
Durmuş, Z., Özdemir, F., Çalışkaner, Z. O., et al. (2025) · Diamond and Related Materials · doi:10.1016/j.diamond.2025.113064 · Cited by 5
Boehme, J. B., Datar, S. A., Sun, X., Gong, W., Lü, Q., Soto, J. E., Smith, M. A., Flores, A. G., Raff, G. W., Wang, T., et al. (2025) · Scientific Reports · doi:10.1038/s41598-025-99062-0 · Cited by 5
“21 Based on our previous findings and observations from other groups, we believe that pulmonary endothelial mitochondria play a central role in integrating and relaying pathologic mechanotransductive signals in the setting of abnormal pulmonary hemodynamics.”
Leucomethylene blue probe detects a broad spectrum of reactive oxygen and nitrogen species
Cremer, C., Merkes, J. M., Bub, C. L., Rommel, D., Patureau, F. W., & Banala, S. (2021) · RSC Advances · doi:10.1039/d1ra06498c · Cited by 5
Retinoids and Reactive Oxygen Species in Cancer Cell Death and Therapeutics
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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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