Role of Glutathione in Cancer Progression and Chemoresistance
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Glutathione (GSH) plays an important role in a multitude of cellular processes, including cell differentiation, proliferation, and apoptosis, and disturbances in GSH homeostasis are involved in the etiology and progression of many human diseases including cancer. While GSH deficiency, or a decrease in the GSH/glutathione disulphide (GSSG) ratio, leads to an increased susceptibility to oxidative stress implicated in the progression of cancer, elevated GSH levels increase the antioxidant capacity and the resistance to oxidative stress as observed in many cancer cells. The present review highlights the role of GSH and related cytoprotective effects in the susceptibility to carcinogenesis and in the sensitivity of tumors to the cytotoxic effects of anticancer agents.
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GSH deficiency is related to the onset and progression of several diseases, including cancer, immunodeficiencies, seizures, neurodegeneration, cardiovascular dysfunctions, and diabetes.
“A GSH deficiency has been related to the onset and progression of several diseases, including cancer, immunodeficiencies, seizures, neurodegeneration, cardiovascular dysfunctions, and diabetes [178,179,180].”
From The Role of Antioxidants in the Interplay between Oxidative Stress and Senescence (2022) · cites this paper as [179]
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- Authors
- Traverso, N., Ricciarelli, R., Nitti, M., Marengo, B., Furfaro, A. L., Pronzato, M. A., Marinari, U. M., & Domenicotti, C.
- Affiliations
- University of Genoa (IT)
- Corresponding author
- Domenicotti, Cinzia
- ORCID
- Venue
- Oxidative Medicine and Cellular Longevity
- Publisher
- Wiley
- Published
- 2013
- Volume
- 2013
- Pages
- 1-10
- ISSN
- 1942-0994 (ISSN-L)
- 1942-0900
- PMC
- PMC3673338
- OpenAlex
- W2096258216
- Cited by
- 1,208
- References
- 126
- Citations by year
- 2026: 81 · 2025: 95 · 2024: 92 · 2023: 135 · 2022: 130 · 2021: 139 · 2020: 130 · 2019: 100 · 2018: 80 · 2017: 82 · 2016: 70 · 2015: 42 · 2014: 25 · 2013: 7
- FWCI
- 4.51
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Locations
- Oxidative Medicine and Cellular Longevity (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- CINECA IRIS Institutial Research Information System (University of Genoa) (submittedVersion)
- Funders
- Ministero dell’Istruzione, dell’Università e della Ricerca (2009M8FKBB_002)
- Università degli Studi di Genova (2009M8FKBB_002)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Glutathione Transferases and Polymorphisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Sulfur Compounds in Biology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Keywords
- glutathione, glutathione disulfide, tumor progression, chemoresistance, oxidative stress, antioxidant capacity, carcinogenesis, anticancer drug sensitivity, cytoprotection
- MeSH terms
- Animals, Glutathione, Humans, Neoplasms, Disease Progression, Drug Resistance, Neoplasm
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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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