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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BackgroundThe phosphoinositide 3-kinase pathway
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Cycling cancer persister cells arise from lineages with distinct programs
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Therapeutic targeting of the hypoxic tumour microenvironment
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Interplay of oxidative stress, cellular communication and signaling pathways in cancer
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BackgroundSex differences in cancer mechanisms
Rubin, J. B., Lagas, J. S., Broestl, L., Sponagel, J., Rockwell, N., Rhee, G., Rosen, S. F., Chen, S., Klein, R. S., Imoukhuede, P. I., et al. (2020) · Biology of Sex Differences · doi:10.1186/s13293-020-00291-x · Cited by 385
Role of cytochrome P450s in the generation and metabolism of reactive oxygen species
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“While ROS is known to contribute to carcinogenesis through increased proliferation and survival, excessive ROS can still lead to cellular damage and cytotoxicity, even in tumor cells [69].”
BackgroundRedox Signaling by Reactive Electrophiles and Oxidants
Parvez, S., Long, M. J. C., Poganik, J. R., & Aye, Y. (2018) · Chemical Reviews · doi:10.1021/acs.chemrev.7b00698 · Cited by 368
An Acquired Vulnerability of Drug-Resistant Melanoma with Therapeutic Potential
Wang, L., de Oliveira, R. L., Huijberts, S. C. F. A., Bosdriesz, E., Pencheva, N., Brunen, D., Bosma, A. R., Song, J., Zevenhoven, J., Vries, G. T. L.-D., et al. (2018) · Cell · doi:10.1016/j.cell.2018.04.012 · Cited by 334
“One of the features of increased RAS signaling is the abundant production of ROS, which serve as signaling molecules in multiple cellular pathways (Lee et al., 1999; Reczek and Chandel, 2017; Ruefli et al., 2001).”
Reactive Oxygen Species (ROS): Key Components in Cancer Therapies
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Emerging mechanisms and targeted therapy of ferroptosis in cancer
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Mitochondrial ROS control of cancer
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Oxidative Stress in the Tumor Microenvironment and Its Relevance to Cancer Immunotherapy
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Reactive oxygen species: a volatile driver of field cancerization and metastasis
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Versatile polyphenolic platforms in regulating cell biology
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Oxidative Stress, Inflammation and Colorectal Cancer: An Overview
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Immune cell - produced ROS and their impact on tumor growth and metastasis
Kennel, K. B., & Greten, F. R. (2021) · Redox Biology · doi:10.1016/j.redox.2021.101891 · Cited by 209
“ROS regulate several critical aspects of tumor biology such as proliferation, resistance to cell death, epithelial-to-mesenchymal transition (EMT) and angiogenesis by interacting with key oncogenic molecular pathways including PI3K/Akt/mTOR, RAS/ERK, JNK/p38, NF-κB, HIF and Src kinase signaling [3,13].”
BackgroundInfluentialMetabolic Modulation of Immunity: A New Concept in Cancer Immunotherapy
Guerra, L., Bonetti, L., & Brenner, D. (2020) · Cell Reports · doi:10.1016/j.celrep.2020.107848 · Cited by 194
“In contrast, malignant cells acquire potent antioxidant capacity that allows ROS to act as pro-tumorigenic signaling molecules (Reczek and Chandel, 2017; Harris et al., 2015) and to stabilize Hif1a (Chandel et al.”
BackgroundDendritic Cell Metabolism and Function in Tumors
Giovanelli, P., Sandoval, T. A., & Cubillos‐Ruiz, J. R. (2019) · Trends in Immunology · doi:10.1016/j.it.2019.06.004 · Cited by 190
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“However, at higher concentrations, an increase in ROS can boost anti-tumorigenic signaling and trigger oxidative stress-induced apoptosis of cancer cells [43].”
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“A consequence of this metabolic reprogramming is increased production of reactive oxygen species (ROS), which must be countered by endogenous antioxidants to avoid loss of cell viability (5).”
BackgroundReactive oxygen species and DNA damage response in cancer
Renaudin, X. (2021) · International review of cytology · doi:10.1016/bs.ircmb.2021.04.001 · Cited by 172
Fu, S., Yang, R., Zhang, L., Liu, W., Du, G., Cao, Y., Xu, Z., Cui, H., Kang, Y., & Xue, P. (2020) · Biomaterials · doi:10.1016/j.biomaterials.2020.120279 · Cited by 163
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The plasticity of pancreatic cancer metabolism in tumor progression and therapeutic resistance
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Redox control in cancer development and progression
Helfinger, V., & Schröder, K. (2018) · Molecular Aspects of Medicine · doi:10.1016/j.mam.2018.02.003 · Cited by 153
Synergistic effect of fasting-mimicking diet and vitamin C against KRAS mutated cancers
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Adhesion-mediated mechanosignaling forces mitohormesis
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“This NRF2-mediated ROS quenching OSR facilitates metabolic remodeling that provides cancer cells with OxSR requisite to harness ROS-mediated proliferation and migration effects without succumbing to ROS-mediated cell death (Reczek and Chandel, 2017).”
Implications of reactive oxygen species on cancer formation and its treatment
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Fenton reaction-based nanomedicine in cancer chemodynamic and synergistic therapy
Meng, X., Zhang, X., Liu, M., Cai, B., He, N., & Wang, Z. (2020) · Applied Materials Today · doi:10.1016/j.apmt.2020.100864 · Cited by 141
ROS Promotes Cancer Cell Survival through Calcium Signaling
Reczek, C. R., & Chandel, N. S. (2018) · Cancer Cell · doi:10.1016/j.ccell.2018.05.010 · Cited by 142
Self-citationStimulus-responsive self-assembled prodrugs in cancer therapy
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Targeting ROS-Mediated Crosstalk Between Autophagy and Apoptosis in Cancer
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A ROS-dependent mechanism promotes CDK2 phosphorylation to drive progression through S phase
Kirova, D., Judasová, K., Vorhauser, J., Zerjatke, T., Leung, J. K., Glauche, I., & Mansfeld, J. (2022) · Developmental Cell · doi:10.1016/j.devcel.2022.06.008 · Cited by 125
“H2O2 is more stable, membrane-permeant, and at physiological concentrations can act as a signaling molecule in a variety of biological processes such as GF signaling, proliferation, differentiation, and adaptation to hypoxia (Holmström and Finkel, 2014; Reczek and Chandel, 2017; Shadel and Horvath, 2015).”
BackgroundPorphyrin‐Based Metal−Organic Framework Compounds as Promising Nanomedicines in Photodynamic Therapy
Yu, W., Zhen, W., Zhang, Q., Yan-chun, L., Luo, H., He, J., & Liu, Y. (2020) · ChemMedChem · doi:10.1002/cmdc.202000353 · Cited by 119
Loenhout, J. V., Flieswasser, T., Boullosa, L. F., Waele, J. D., Audenaerde, J. R. M. V., Marcq, E., Jacobs, J., Lin, A. G., Lion, E., Dewitte, H., et al. (2019) · Cancers · doi:10.3390/cancers11101597 · Cited by 122
“This altered redox environment can increase their susceptibility to ROS-promoting therapies like pPBS by disturbing ROS homeostasis, resulting in lethal ROS levels and ultimately cancer cell death [42].”
BackgroundMedicinal Prospects of Antioxidants From Algal Sources in Cancer Therapy
Ferdous, U. T., & Yusof, Z. N. B. (2021) · Frontiers in Pharmacology · doi:10.3389/fphar.2021.593116 · Cited by 121
“Conversely, elevated ROS level promotes oxidative stress-induced cancer cell death by triggering antitumorigenic signaling (Reczek and Chandel, 2017; Kashyap et al., 2019).”
BackgroundPolymersome-based protein drug delivery – quo vadis?
Gouveia, M. G., Wesseler, J. P., Ramaekers, J., Weder, C., Scholten, P. B. V., & Bruns, N. (2022) · Chemical Society Reviews · doi:10.1039/d2cs00106c · Cited by 119
Ma’ayan, A. (2017) · Journal of The Royal Society Interface · doi:10.1098/rsif.2017.0391 · Cited by 120
Liu, R., Bian, Y., Liu, L., Liu, L., Liu, X., & Ma, S. (2022) · International Journal of Molecular Medicine · doi:10.3892/ijmm.2022.5121 · Cited by 119
“(29).”
D’Angelo, S., Martino, E., Ilisso, C. P., Bagarolo, M. L., Porcelli, M., & Cacciapuoti, G. (2017) · International Journal of Oncology · doi:10.3892/ijo.2017.4088 · Cited by 109
“It has been shown that lipid hydroperoxides as well as lipid peroxidation initiators, such as ROS, are involved in signaling pathways that control cell proliferation, differentiation, maturation, and apoptosis (1,27).”
BackgroundYu, Y., Pan, M., Peng, J., et al. (2022) · Chinese Chemical Letters · doi:10.1016/j.cclet.2022.02.045 · Cited by 105
Lunetti, P., Giacomo, M. D., Vergara, D., Domenico, S. D., Maffia, M., Zara, V., Capobianco, L., & Ferramosca, A. (2019) · FEBS Journal · doi:10.1111/febs.14756 · Cited by 106
Zhao, Y., Liu, J., He, M., Dong, Q., Zhang, L., Xu, Z., Kang, Y., & Xue, P. (2022) · ACS Nano · doi:10.1021/acsnano.2c02540 · Cited by 102
Wang, X., Li, Y., Li, Z., Lin, S., Wang, H., Sun, J., Lan, C., Wu, L., Sun, D., Huang, C., et al. (2022) · Cancer Research · doi:10.1158/0008-5472.can-21-3230 · Cited by 105
Blockade of Glutathione Metabolism in IDH1 -Mutated Glioma
Tang, X., Fu, X., Liu, Y., Yu, D., Cai, S. J., & Yang, C. (2019) · Molecular Cancer Therapeutics · doi:10.1158/1535-7163.mct-19-0103 · Cited by 100
“17 IDH-mutated cells develop dependency on glutathione ROS scavenging 1 The production of ROS is involved in several aspects of cancer biology, such as genomic 2 instability, loss of growth control, cellular motility, and tumor invasiveness (35,36).”
BackgroundNanoceria: an innovative strategy for cancer treatment
Tang, J., Moonshi, S. S., & Ta, H. T. (2023) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-023-04694-y · Cited by 100
“Further studies suggested that ROS have a dual role in cancer tumorigenesis and cancer cell survival via: (1) increased ROS production promoting pro-tumourigenic signalling events to facilitate cancer cell proliferation, metastasis, angiogenesis and adapting to hypoxia resulting in aggressive tumour growth; (2) reinfo…”
BackgroundInteractions of multidomain pro-apoptotic and anti-apoptotic proteins in cancer cell death
Chota, A., George, B. P. A., & Abrahamse, H. (2021) · Oncotarget · doi:10.18632/oncotarget.28031 · Cited by 106
“Therefore, it is critical for researchers involved in the development of better therapeutic options to consider optimizing the levels of ROS to be generated during therapy as it prevents proliferation and cancer recurrence [14].”
BackgroundInfluentialRecent advances in redox-responsive nanoparticles for combined cancer therapy
Yang, Y., & Sun, W. C. (2022) · Nanoscale Advances · doi:10.1039/d2na00222a · Cited by 98
Reactive Oxygen Species: Not Omnipresent but Important in Many Locations
Herb, M., Gluschko, A., & Schramm, M. (2021) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2021.716406 · Cited by 93
New strategies to treat AML: novel insights into AML survival pathways and combination therapies
Nair, R., Salinas-Illarena, A., & Baldauf, H. (2020) · Leukemia · doi:10.1038/s41375-020-01069-1 · Cited by 86
“The role of ROS in cancer is bifunctional and heavily dependent on the levels of these radicals, the ability of the cell to cope with them, and the downstream pathways that are involved [63].”
BackgroundTrimodal synergistic antitumor drug delivery system based on graphene oxide
Zhang, X., Luo, L., Li, L., He, Y., Cao, W., Liu, H., Niu, K., & Gao, D. (2018) · Nanomedicine Nanotechnology Biology and Medicine · doi:10.1016/j.nano.2018.09.008 · Cited by 85
Azzi, A. (2022) · Antioxidants · doi:10.3390/antiox11081431 · Cited by 83
Ernst, L. M., Casals, E., Italiani, P., Boraschi, D., & Puntes, V. (2021) · Nanomaterials · doi:10.3390/nano11112991 · Cited by 92
“ROS are free radical molecules resulting from natural metabolism, which, when excessive and unregulated, may contribute to cell damage and aggravate human pathologies such as cancer [5], neurodegeneration, and stroke, among others [6].”
BackgroundPontel, L. B., Bueno-Costa, A., Morellato, A. E., Santos, J. C., Roué, G., & Esteller, M. (2022) · Redox Biology · doi:10.1016/j.redox.2022.102408 · Cited by 82
“GPX4-inhibition in conditions of FSP1 overexpression might lead to an increase in reactive oxygen species (ROS), which are not able to kill the cells (because of the presence of FSP1) but can promote growth as previously shown for canonical ROS [41].”
BackgroundLi, X., Rommelaere, S., Kondo, S., & Lemaître, B. (2020) · Immunity · doi:10.1016/j.immuni.2020.01.008 · Cited by 78
Small-Molecule Inhibitors of Reactive Oxygen Species Production
Sassetti, E., Clausen, M. H., & Laraia, L. (2021) · Journal of Medicinal Chemistry · doi:10.1021/acs.jmedchem.0c01914 · Cited by 85
Venn diagram analysis overestimates the extent of circadian rhythm reprogramming
Pelikan, A., Herzel, H., Kramer, A., & Ananthasubramaniam, B. (2021) · FEBS Journal · doi:10.1111/febs.16095 · Cited by 79
“We propose that the complex interaction between redox balance and cancer [23] is also circadian clock mediated with a possible role for blood vessel development.”
BackgroundVo, T. T. T., Vo, Q. C., Tuan, V. P., Wee, Y., Cheng, J. H.-C., & Lee, I. (2021) · Redox Biology · doi:10.1016/j.redox.2021.102124 · Cited by 81
“Pro-tumorigenic pathways are accompanied by higher levels of ROS, but anti-tumorigenic pathways may occur under excessive oxidative burden, suggesting the dual role of ROS in cancer [96].”
BackgroundFighting in a wasteland: deleterious metabolites and antitumor immunity
Watson, M. J., & Delgoffe, G. M. (2022) · Journal of Clinical Investigation · doi:10.1172/jci148549 · Cited by 83
“ROS production in the TME is finely tuned by ROS generators and ROS scavengers to maintain optimal levels for signaling, growth, and survival (80).”
BackgroundThe gate to metastasis: key players in cancer cell intravasation
Sznurkowska, M. K., & Aceto, N. (2021) · FEBS Journal · doi:10.1111/febs.16046 · Cited by 86
Methionine oxidation activates pyruvate kinase M2 to promote pancreatic cancer metastasis
He, D., Feng, H., Sundberg, B., Yang, J., Powers, J., Christian, A. H., Wilkinson, J. E., Monnin, C., Avizonis, D. Z., Thomas, C. J., et al. (2022) · Molecular Cell · doi:10.1016/j.molcel.2022.06.005 · Cited by 80
“Although reactive oxygen species (ROS) have been implicated in tumor development, the fundamental relationships between redox biology and cancer remain poorly understood (Reczek and Chandel, 2017).”
BackgroundDeng, J., Pan, T., Liu, Z., McCarthy, C., Vicencio, J. M., Cao, L., Alfano, G., Suwaidan, A. A., Yin, M., Beatson, R., et al. (2023) · British Journal of Cancer · doi:10.1038/s41416-023-02442-4 · Cited by 77
“Notably, the dual role of ROS in cancer could partially be the reason for diverse functions of TXNIP in cancer [76].”
Martino, E., Vuoso, D. C., D’Angelo, S., Mele, L. L., D’Onofrio, N., Porcelli, M., & Cacciapuoti, G. (2019) · Scientific Reports · doi:10.1038/s41598-019-49631-x · Cited by 75
Responsive triggering systems for delivery in chronic wound healing
Morey, M., & Pandit, A. S. (2018) · Advanced Drug Delivery Reviews · doi:10.1016/j.addr.2018.02.008 · Cited by 76
Kim, Y., Uthaman, S., Pillarisetti, S., Noh, K., Huh, K. M., & Park, I. (2020) · Acta Biomaterialia · doi:10.1016/j.actbio.2020.03.027 · Cited by 71
Wu, C., Tan, X., Hu, X., Zhou, M., Yan, J., & Ding, C. (2019) · The Journal of Immunology · doi:10.4049/jimmunol.1900930 · Cited by 70
Oxidative Stress Inducers in Cancer Therapy: Preclinical and Clinical Evidence
Nizami, Z. N., Aburawi, H. E., Semlali, A., Muhammad, K., & Iratni, R. (2023) · Antioxidants · doi:10.3390/antiox12061159 · Cited by 78
“Physiologically, ROS are produced as byproducts of metabolic reactions, namely electron leakage during oxidative phosphorylation in the mitochondria, through the activity of NADPH oxidases, and via the iron-dependent Fenton reaction [2,3].”
BackgroundInfluentialOptimized strategies of ROS-based nanodynamic therapies for tumor theranostics
Di, Y., Deng, R., Liu, Z., Mao, Y., Gao, Y., Zhao, Q., & Wang, S. (2023) · Biomaterials · doi:10.1016/j.biomaterials.2023.122391 · Cited by 71
Ding, Y., Yu, J., Chen, X., Wang, S., Tu, Z., Shen, G., Wang, H., Jia, R., Ge, S., Ruan, J., et al. (2021) · Advanced Science · doi:10.1002/advs.202002404 · Cited by 66
Crosstalk Between ROS and Autophagy in Tumorigenesis: Understanding the Multifaceted Paradox
Hasan, A., Rizvi, S. F., Parveen, S., Pathak, N., Nazir, A., & Mir, S. S. (2022) · Frontiers in Oncology · doi:10.3389/fonc.2022.852424 · Cited by 77
“• Oxidative modification of PTEN • Oncogenic stabilization of hypoxia-inducible factor (HIF)-1a; conversion to hydroxyl radical (50; 51, 52)”
BackgroundInterplay of oxidative stress and antioxidant mechanisms in cancer development and progression
Jomová, K., Alomar, S. Y., Valko, R., Fresser, L., Nepovimová, E., Kuča, K., & Valko, M. (2025) · Archives of Toxicology · doi:10.1007/s00204-025-04146-5 · Cited by 103
“A variety of ROS, especially their prominent member H 2 O 2 , operating within physiological limits, are central players in redox signaling; however, when upregulated, ROS may act as damaging species capable of reversibly oxidizing the cysteine side chains of proteins (Reczek And Chandel 2017).”
Kavalappa, Y. P., Gopal, S. S., & Ponesakki, G. (2020) · Journal of Cellular Physiology · doi:10.1002/jcp.29961 · Cited by 69
“Considering the proliferation and survival of cancer cells rely on the signaling capabilities of ROS (Reczek & Chandel, 2017), disruption of ROS homeostasis in breast cancer cells by lutein in the present study might influence on cell survival signaling.”
BackgroundFuloria, S., Subramaniyan, V., Sundram, K., Kumari, U., Sathasivam, K. V., Meenakshi, D. U., Wu, Y. S., Sekar, M., Chitranshi, N., Malviya, R., et al. (2021) · Antioxidants · doi:10.3390/antiox10010128 · Cited by 77
“Cancer cells (CC) analysis suggests that ROS in high levels cause damage of cell components (proteins, lipids, and DNA), oncogenicity, genome instability, and tumorigenesis [3,4].”
BackgroundNUPR1: A Critical Regulator of the Antioxidant System
Huang, C., Santofimia‐Castaño, P., & Iovanna, J. (2021) · Cancers · doi:10.3390/cancers13153670 · Cited by 67
“Regardless of histological type, all tumor cells have excessively high ROS levels and powerful antioxidant systems, which protect against oxidative damage [106,107].”
BackgroundRomashev, N. F., Abramov⧫, P. A., Bakaev⧫, I. V., et al. (2022) · Inorganic Chemistry · doi:10.1021/acs.inorgchem.1c03314 · Cited by 64
Targeted Anti-Mitochondrial Therapy: The Future of Oncology
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Tamamouna, V., Rahman, M. M., Petersson, M., Charalambous, I., Kux, K., Mainor, H., Bolender, V., Isbilir, B., Edgar, B. A., & Pitsouli, C. (2021) · Nature Cell Biology · doi:10.1038/s41556-021-00674-1 · Cited by 57
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Yu, X. Q., Huang, Y., Tao, Y., Fan, L., & Zhang, Y. (2023) · Analytica Chimica Acta · doi:10.1016/j.aca.2023.342060 · Cited by 62
CD146‐Targeted Multimodal Image‐Guided Photoimmunotherapy of Melanoma
Wei, W., Jiang, D., Ehlerding, E. B., Barnhart, T. E., Yang, Y., Engle, J. W., Luo, Q., Huang, P., & Cai, W. (2019) · Advanced Science · doi:10.1002/advs.201801237 · Cited by 59
Modulating intracellular oxidative stress via engineered nanotherapeutics
Hu, J., & Liu, S. (2019) · Journal of Controlled Release · doi:10.1016/j.jconrel.2019.12.040 · Cited by 60
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Antioxidant responses related to temozolomide resistance in glioblastoma
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“1), could be an effective anticancer approach (Pelicano et al., 2004; Reczek and Chandel, 2017).”
BackgroundNLRP3 and cancer: Pathogenesis and therapeutic opportunities
Tengesdal, I. W., Dinarello, C. A., & Marchetti, C. (2023) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2023.108545 · Cited by 69
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“The main sources of ROS in aerobic cells can be related to membrane-bound NADPH oxidase and to incomplete oxygen reduction in mitochondria [3].”
BackgroundLi, X., Chen, Y., Zhao, J., Shi, J., Wang, M., Qiu, S., Hu, Y., Xu, Y., Cui, Y., Liu, C., et al. (2019) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2019/9706792 · Cited by 64
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A Nonenzymatic Hydrogen Peroxide Electrochemical Sensing and Application in Cancer Diagnosis
Yu, Y., Peng, J., Pan, M., Yang, M. S., Li, Y., Yuan, L., Liu, Q., Han, R., Hao, Y., Yang, Y., et al. (2021) · Small Methods · doi:10.1002/smtd.202001212 · Cited by 54
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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