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Redox-Directed Cancer Therapeutics: Molecular Mechanisms and Opportunities
Open accessAbstract
Redox dysregulation originating from metabolic alterations and dependence on mitogenic and survival signaling through reactive oxygen species represents a specific vulnerability of malignant cells that can be selectively targeted by redox chemotherapeutics. This review will present an update on drug discovery, target identification, and mechanisms of action of experimental redox chemotherapeutics with a focus on pro- and antioxidant redox modulators now in advanced phases of preclinal and clinical development. Recent research indicates that numerous oncogenes and tumor suppressor genes exert their functions in part through redox mechanisms amenable to pharmacological intervention by redox chemotherapeutics. The pleiotropic action of many redox chemotherapeutics that involves simultaneous modulation of multiple redox sensitive targets can overcome cancer cell drug resistance originating from redundancy of oncogenic signaling and rapid mutation.Moreover, some redox chemotherapeutics may function according to the concept of synthetic lethality (i.e., drug cytotoxicity is confined to cancer cells that display loss of function mutations in tumor suppressor genes or upregulation of oncogene expression). The impressive number of ongoing clinical trials that examine therapeutic performance of novel redox drugs in cancer patients demonstrates that redox chemotherapy has made the crucial transition from bench to bedside.
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“current pro-oxidant strategies often cause serious collateral damage, resulting in a narrow therapeutic window20”
From Targeting cancer vulnerabilities with high-dose vitamin C (2019) · cites this paper as [20]
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2 retracted
Suliman, H. B., Carraway, M. S., Ali, A. S., Reynolds, C. M., Welty‐Wolf, K. E., & Piantadosi, C. A. (2007) · Journal of Clinical Investigation · doi:10.1172/jci32967 · Cited by 261
RetractedGong, X., Kole, L., Iskander, K. S., & Jaiswal, A. K. (2007) · Cancer Research · doi:10.1158/0008-5472.can-07-0323 · Cited by 107
RetractedSchafer, F. Q., & Buettner, G. R. (2001) · Free Radical Biology and Medicine · doi:10.1016/s0891-5849(01)00480-4 · Cited by 4,587
Targeting cancer with small molecule kinase inhibitors
Zhang, J., Yang, P. L., & Gray, N. S. (2008) · Nature reviews. Cancer · doi:10.1038/nrc2559 · Cited by 2,648
Production of large amounts of hydrogen peroxide by human tumor cells.
Szatrowski, T. P., & Nathan, C. (1991) · PubMed · Cited by 2,504
Mammalian thioredoxin is a direct inhibitor of apoptosis signal‐regulating kinase (ASK) 1
Saitoh, M., Nishitoh, H., Fujii, M., Takeda, K., Tobiume, K., Sawada, Y., Kawabata, M., Miyazono, K., & Ichijo, H. (1998) · The EMBO Journal · doi:10.1093/emboj/17.9.2596 · Cited by 2,377
TIGAR, a p53-Inducible Regulator of Glycolysis and Apoptosis
Bensaad, K., Tsuruta, A., Selak, M. A., Vidal, M. N. C., Nakano, K., Bartrons, R., Gottlieb, E., & Vousden, K. H. (2006) · Cell · doi:10.1016/j.cell.2006.05.036 · Cited by 2,019
Yang, W. S., & Stockwell, B. R. (2008) · Chemistry & Biology · doi:10.1016/j.chembiol.2008.02.010 · Cited by 1,876
Redox regulation of cell survival
Trachootham, D., Lu, W., Ogasawara, M. A., Valle, N. R.-D., & Huang, P. (2008) · Antioxidants & Redox Signaling · doi:10.1089/ars.2007.1957 · Cited by 1,781
p53 Regulates Mitochondrial Respiration
Matoba, S., Kang, J.-G., Patino, W. D., Wragg, A., Boehm, M., Gavrilova, O., Hurley, P. J., Bunz, F., & Hwang, P. M. (2006) · Science · doi:10.1126/science.1126863 · Cited by 1,650
Research works printed but not linked: 31
- Adachi M, 2007, Histol Histopathol, 22, 437
- Bahlis NJ, 2002, Clin Cancer Res, 8, 3658
- Berger TG, 2005, Oncol Rep, 14, 1599
- Brown JM, 2007, Methods Enzymol, 435, 297
- Cabello CM, 2007, Curr Opin Investig Drugs, 8, 1022
- Chang HS, 2007, Int J Oncol, 30, 1129
- Cullen JJ, 2003, Cancer Res, 63, 5513
- Efferth T, 2003, Int J Oncol, 23, 1231
- Fang J, 2003, Cancer Res, 63, 3567
- Filomeni G, 2003, Cancer Res, 63, 5940
- Foldi M, 2007, Oncol Rep, 17, 841
- Gallegos A, 1996, Cancer Res, 56, 5765
- Guo J, 2007, Anticancer Res, 27, 3067
- Kakolyris S, 2001, Clin Cancer Res, 7, 3087
- Kirkpatrick DL, 1997, Oncol Res, 9, 351
- Lopez–Lazaro M, 2008, Mol Nutr Food Res 52 Suppl, 1, S103
- Luo M, 2004, Anticancer Res, 24, 2127
- Nonn L, 2003, Mol Cancer Res, 1, 682
- Pan JG, 2007, Sci STKE, 2007, pe14
- Pan XQ, 2007, In vivo, 21, 259
- Shankar S, 2007, Int J Oncol, 30, 905
- Singh NP, 2004, Anticancer Res, 24, 2277
- Stephenson CM, 2007, J Am Osteopath Assoc, 107, 212
- Suliman HB, 2007, J Clin Invest, 117, 3730
- Szatrowski TP, 1991, Cancer Res, 51, 794
- Thimmulappa RK, 2002, Cancer Res, 62, 5196
- von Eschenbach AC, 2003, J Natl Med Assoc, 95, 637
- Welsh SJ, 2002, Cancer Res, 62, 5089
- Welsh SJ, 2003, Mol Cancer Ther, 2, 235
- Wu Y, 2004, Anticancer Res, 24, 3795
- 10.1158/0008-5472.CAN-04-4313 · DOI
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NRF2 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
Role of Glutathione in Cancer Progression and Chemoresistance
Traverso, N., Ricciarelli, R., Nitti, M., Marengo, B., Furfaro, A. L., Pronzato, M. A., Marinari, U. M., & Domenicotti, C. (2013) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2013/972913 · Cited by 1,208
Targeting cancer vulnerabilities with high-dose vitamin C
Ngo, B., Van Riper, J. M., Cantley, L. C., & Yun, J. (2019) · Nature Reviews Cancer · doi:10.1038/s41568-019-0135-7 · Cited by 423
Kell, D. B. (2010) · Archives of Toxicology · doi:10.1007/s00204-010-0577-x · Cited by 361
On the history of oxidative stress: Concept and some aspects of current development
Sies, H. (2018) · Current Opinion in Toxicology · doi:10.1016/j.cotox.2018.01.002 · Cited by 285
Thiol regulation by Mn porphyrins, commonly known as SOD mimics
Batinic-Haberle, I., & Tome, M. E. (2019) · Redox Biology · doi:10.1016/j.redox.2019.101139 · Cited by 88
Ma, J., Lim, C., Sacher, J. R., Van Houten, B., Qian, W., & Wipf, P. (2015) · Bioorganic & Medicinal Chemistry Letters · doi:10.1016/j.bmcl.2015.06.073 · Cited by 27
Mangiferin in human disease: Multifaceted mechanisms and applications (Review)
Dai, Y., Huang, Q., Tan, M., Wang, Z., Jiang, C., Liu, Z., Zhang, S., & Song, S. (2026) · International Journal of Molecular Medicine · doi:10.3892/ijmm.2026.5736 · Cited by 3
“…proposed by previous scholars, these strategies effectively integrate formulation, dosage and Pds into a coherent translational framework (166,195,197). deeper investigations into signaling pathways, including the NF‑ κ B, Nrf2 and AMPK pathways, will further clarify the underlying mechanisms of…”
Metadata
- Authors
- Wondrak, G. T.
- Affiliations
- University of Arizona (US)
- Corresponding author
- Wondrak, Georg T.
- ORCID
- Wondrak, Georg T.
- Venue
- Antioxidants & Redox Signaling
- Publisher
- SAGE Publications
- Published
- 2009-12
- Volume
- 11
- Issue
- 12
- Pages
- 3013-3069
- ISSN
- 1523-0864 (ISSN-L)
- 1557-7716
- PMC
- PMC2824519
- OpenAlex
- W2000718634
- Cited by
- 462
- References
- 406
- Citations by year
- 2026: 7 · 2025: 24 · 2024: 16 · 2023: 18 · 2022: 18 · 2021: 23 · 2020: 25 · 2019: 29 · 2018: 26 · 2017: 35 · 2016: 44 · 2015: 42 · 2014: 40 · 2013: 33 · 2012: 34
- FWCI
- 2.09
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Antioxidants and Redox Signaling (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- University of Arizona Cancer Center (CA023074)
- Servier
- National Institutes of Health (CA023074, ES 06694)
- National Cancer Institute (R01CA122484, CA-023074, P30CA023074)
- National Institute of Environmental Health Sciences (ES 06694, P30ES006694)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Toxicology › Bioactive Compounds and Antitumor Agents
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cancer and biochemical research
- Keywords
- reactive oxygen species, redox dysregulation, cancer cell vulnerability, oncogene function, tumor suppressor, chemoresistance, synthetic lethality, redox signaling, drug discovery, clinical trials
- MeSH terms
- Antineoplastic Agents, Humans, Neoplasms, Oxidation-Reduction
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