Cited by 2,760Metal complexes synthesis and propertiesDNA Repair MechanismsCancer therapeutics and mechanisms

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Molecular mechanisms of cisplatin resistance

Galluzzi, L, Senovilla, L, Vitale, I, Michels, J, Martins, I, Kepp, O, Castedo, M, Kroemer, G·2012·Oncogene

DOI 10.1038/onc.2011.384

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Abstract

Platinum-based drugs, and in particular cis-diamminedichloroplatinum(II) (best known as cisplatin), are employed for the treatment of a wide array of solid malignancies, including testicular, ovarian, head and neck, colorectal, bladder and lung cancers. Cisplatin exerts anticancer effects via multiple mechanisms, yet its most prominent (and best understood) mode of action involves the generation of DNA lesions followed by the activation of the DNA damage response and the induction of mitochondrial apoptosis. Despite a consistent rate of initial responses, cisplatin treatment often results in the development of chemoresistance, leading to therapeutic failure. An intense research has been conducted during the past 30 years and several mechanisms that account for the cisplatin-resistant phenotype of tumor cells have been described. Here, we provide a systematic discussion of these mechanism by classifying them in alterations (1) that involve steps preceding the binding of cisplatin to DNA (pre-target resistance), (2) that directly relate to DNA-cisplatin adducts (on-target resistance), (3) concerning the lethal signaling pathway(s) elicited by cisplatin-mediated DNA damage (post-target resistance) and (4) affecting molecular circuitries that do not present obvious links with cisplatin-elicited signals (off-target resistance). As in some clinical settings cisplatin constitutes the major therapeutic option, the development of chemosensitization strategies constitute a goal with important clinical implications.

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RETRACTED ARTICLE: An apoptosis-enhancing drug overcomes platinum resistance in a tumour-initiating subpopulation of ovarian cancer
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Retracted

Authors: Galluzzi, L., Senovilla, L., Vitale, I., Michels, J., Martins, I., Kepp, O., Castedo, M., & Kroemer, G.
Affiliations: Inserm (FR)
Université Paris-Sud (FR)
Corresponding author: Kroemer, G
ORCID: Galluzzi, L
Senovilla, L
Vitale, I
Michels, J
Martins, I
Kepp, O
Castedo, M
Kroemer, G
Venue: Oncogene
Publisher: Springer Science and Business Media LLC
Published: 2011-09-05
Volume: 31
Issue: 15
Pages: 1869-1883
ISSN: 0950-9232 (ISSN-L)
1476-5594
DOI: 10.1038/onc.2011.384
OpenAlex: W2141037581
Cited by: 2,760
References: 196
Citations by year: 2026: 154 · 2025: 187 · 2024: 244 · 2023: 220 · 2022: 247 · 2021: 308 · 2020: 252 · 2019: 213 · 2018: 169 · 2017: 167 · 2016: 159 · 2015: 160 · 2014: 145 · 2013: 89 · 2012: 44
FWCI: 7.83
Type: journal article
Language: en
Open access: closed
Licence: www.springer.com/tdm (tdm)
www.springer.com/tdm (vor)
Locations: Oncogene (publishedVersion)
PubMed (publishedVersion)
Funders: European Commission
Ligue Contre le Cancer
Fondation Bettencourt Schueller
Labex Immuno-Oncology
Topics: Health Sciences › Medicine › Oncology › Metal complexes synthesis and properties
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cancer therapeutics and mechanisms
Keywords: cisplatin resistance, chemoresistance, platinum anticancer drugs, DNA damage response, mitochondrial apoptosis, chemosensitization, DNA lesions
MeSH terms: Cisplatin, DNA Damage, DNA Repair, Humans, Signal Transduction, DNA Adducts, Drug Resistance, Neoplasm

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