The DOI matches its Crossref record; 218 of the 218 references it cites were found in a registry or an index.
Redox Homeostasis and Cellular Antioxidant Systems: Crucial Players in Cancer Growth and Therapy
Open accessAbstract
Reactive oxygen species (ROS) and their products are components of cell signaling pathways and play important roles in cellular physiology and pathophysiology. Under physiological conditions, cells control ROS levels by the use of scavenging systems such as superoxide dismutases, peroxiredoxins, and glutathione that balance ROS generation and elimination. Under oxidative stress conditions, excessive ROS can damage cellular proteins, lipids, and DNA, leading to cell damage that may contribute to carcinogenesis. Several studies have shown that cancer cells display an adaptive response to oxidative stress by increasing expression of antioxidant enzymes and molecules. As a double‐edged sword, ROS influence signaling pathways determining beneficial or detrimental outcomes in cancer therapy. In this review, we address the role of redox homeostasis in cancer growth and therapy and examine the current literature regarding the redox regulatory systems that become upregulated in cancer and their role in promoting tumor progression and resistance to chemotherapy.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
1 retracted
Rosato, R. R., Kolla, S. S., Hock, S. K., Almenara, J. A., Patel, A. K., Amin, S., Atadja, P. W., Fisher, P. B., Dent, P., & Grant, S. (2010) · Journal of Biological Chemistry · doi:10.1074/jbc.m109.095208 · Cited by 65
RetractedMcCord, J. M., & Fridovich, I. (1969) · Journal of Biological Chemistry · doi:10.1016/s0021-9258(18)63504-5 · Cited by 12,952
Targeting HIF-1 for cancer therapy
Semenza, G. L. (2003) · Nature Reviews Cancer · doi:10.1038/nrc1187 · Cited by 6,717 · cited 1×
“It has been demonstrated that HIF-1α interacts with the HIF-1β and acts as a transcription factor able to induce the expression of genes involved in metabolic adaptation, such as hexokinase II (HK II) and pyruvate dehydrogenase kinase 1 (PDK1) [216], and the expression of genes involved in improving oxygen availabilit…”
BackgroundWang, G. L., Jiang, B. H., Rue, E. A., & Semenza, G. L. (1995) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.92.12.5510 · Cited by 6,212
Mdm2 promotes the rapid degradation of p53
Haupt, Y., Maya, R., Kazaz, A., & Oren, M. (1997) · Nature · doi:10.1038/387296a0 · Cited by 4,506
Modulation of oxidative stress as an anticancer strategy
Gorrini, C., Harris, I. S., & Mak, T. W. (2013) · Nature Reviews Drug Discovery · doi:10.1038/nrd4002 · Cited by 3,579
Crosstalk of reactive oxygen species and NF-κB signaling
Morgan, M. J., & Liu, Z.-G. (2011) · Cell Research · doi:10.1038/cr.2010.178 · Cited by 3,505
Targeting hypoxia in cancer therapy
Wilson, W. R., & Hay, M. P. (2011) · Nature Reviews Cancer · doi:10.1038/nrc3064 · Cited by 3,172
Improved Overall Survival in Melanoma with Combined Dabrafenib and Trametinib
Robert, C., Karaszewska, B., Schachter, J., Rutkowski, P., Mackiewicz, A., Stroiakovski, D., Lichinitser, M., Dummer, R., Grange, F., Mortier, L., et al. (2015) · New England Journal of Medicine · doi:10.1056/nejmoa1412690 · Cited by 2,701
Nordberg, J., & Arnér, E. S. J. (2001) · Free Radical Biology and Medicine · doi:10.1016/s0891-5849(01)00724-9 · Cited by 2,662
Cited by
ROS and the DNA damage response in cancer
Srinivas, U. S., Tan, B. W. Q., Vellayappan, B. A., & Jeyasekharan, A. D. (2019) · Redox Biology · doi:10.1016/j.redox.2018.101084 · Cited by 2,144
“Secondly, ROS has a dose dependent effect on activity of proteins leading to differential downstream outcomes [140], which are”
BackgroundNRF2 and the Hallmarks of Cancer
Rojo de la Vega, M., Chapman, E., & Zhang, D. D. (2018) · Cancer Cell · doi:10.1016/j.ccell.2018.03.022 · Cited by 1,672
ROS signaling under metabolic stress: cross-talk between AMPK and AKT pathway
Zhao, Y., Hu, X., Liu, Y., Dong, S., Wen, Z., He, W., Zhang, S., Huang, Q., & Shi, M. (2017) · Molecular Cancer · doi:10.1186/s12943-017-0648-1 · Cited by 735
Impact of Reactive Species on Amino Acids—Biological Relevance in Proteins and Induced Pathologies
Andrés, C. M. C., Pérez de la Lastra, J. M., Andrés Juan, C., Plou, F. J., & Pérez-Lebeña, E. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms232214049 · Cited by 71
Hypoxic microenvironment in cancer: role in metabolic reprogramming
Sureka, N., Maheshwari, R., Agravat, A., Singhal, S., Zaman, S., Rishi, B., Siraj, F., Zaheer, S., & Misra, A. (2026) · Frontiers in Oncology · doi:10.3389/fonc.2026.1771365 · Cited by 11
Metadata
- Authors
- Marengo, B., Nitti, M., Furfaro, A. L., Colla, R., Ciucis, C. D., Marinari, U. M., Pronzato, M. A., Traverso, N., & Domenicotti, C.
- Venue
- Oxidative Medicine and Cellular Longevity
- Publisher
- Wiley
- Published
- 2016-01
- Volume
- 2016
- Issue
- 1
- Pages
- 6235641-6235641
- ISSN
- 1942-0994 (ISSN-L)
- 1942-0900
- OpenAlex
- W2468344619
- Cited by
- 319
- References
- 218
- FWCI
- 13.24
- Type
- journal article
- Language
- en
- Open access
- hybrid
About these checks
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.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
How to cite
Cite CoChat for the checks on this page, and the paper for its own findings.
- This page
- CoChat. (2026). Citation check: Redox Homeostasis and Cellular Antioxidant Systems: Crucial Players in Cancer Growth and Therapy. https://app.cochat.ai/papers/10.1155/2016/6235641
- The paper
- Marengo, B., Nitti, M., Furfaro, A. L., Colla, R., Ciucis, C. D., Marinari, U. M., Pronzato, M. A., Traverso, N., & Domenicotti, C. (2016). Redox Homeostasis and Cellular Antioxidant Systems: Crucial Players in Cancer Growth and Therapy. Oxidative Medicine and Cellular Longevity. https://doi.org/10.1155/2016/6235641
Data sources
Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
