Systems biology of cisplatin resistance: past, present and future
Open accessAbstract
The platinum derivative cis-diamminedichloroplatinum(II), best known as cisplatin, is currently employed for the clinical management of patients affected by testicular, ovarian, head and neck, colorectal, bladder and lung cancers. For a long time, the antineoplastic effects of cisplatin have been fully ascribed to its ability to generate unrepairable DNA lesions, hence inducing either a permanent proliferative arrest known as cellular senescence or the mitochondrial pathway of apoptosis. Accumulating evidence now suggests that the cytostatic and cytotoxic activity of cisplatin involves both a nuclear and a cytoplasmic component. Despite the unresolved issues regarding its mechanism of action, the administration of cisplatin is generally associated with high rates of clinical responses. However, in the vast majority of cases, malignant cells exposed to cisplatin activate a multipronged adaptive response that renders them less susceptible to the antiproliferative and cytotoxic effects of the drug, and eventually resume proliferation. Thus, a large fraction of cisplatin-treated patients is destined to experience therapeutic failure and tumor recurrence. Throughout the last four decades great efforts have been devoted to the characterization of the molecular mechanisms whereby neoplastic cells progressively lose their sensitivity to cisplatin. The advent of high-content and high-throughput screening technologies has accelerated the discovery of cell-intrinsic and cell-extrinsic pathways that may be targeted to prevent or reverse cisplatin resistance in cancer patients. Still, the multifactorial and redundant nature of this phenomenon poses a significant barrier against the identification of effective chemosensitization strategies. Here, we discuss recent systems biology studies aimed at deconvoluting the complex circuitries that underpin cisplatin resistance, and how their findings might drive the development of rational approaches to tackle this clinically relevant problem.
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Mitotic catastrophe is a major mechanism of action of anticancer chemotherapeutics, reflecting increased resistance of neoplastic cells to intrinsic apoptosis.
“However, mitotic catastrophe appears to constitute a major mechanism of action of anticancer chemotherapeutics, mostly reflecting the increased resistance of neoplastic cells to the induction of intrinsic apoptosis [1004–1009].”
From Molecular mechanisms of cell death: recommendations of the nomenclature committee on cell death 2018. (2018) · cites this paper as [1008]
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- Authors
- Galluzzi, L., Vitale, I., Michels, J., Brenner, C., Szabadkai, G., Harel-Bellan, A., Castedo, M., & Kroemer, G.
- Affiliations
- Institut Gustave Roussy (FR)
- Istituto Superiore di Sanità (IT)
- Inserm (FR)
- University of Padua (IT)
- Corresponding author
- Galluzzi, L
- Kroemer, G
- Venue
- Cell Death & Disease
- Published
- 2014-05-29
- Volume
- 5
- Issue
- 5
- Pages
- e1257-e1257
- ISSN
- 2041-4889 (ISSN-L)
- PMC
- PMC4047912
- OpenAlex
- W2019156893
- Cited by
- 782
- References
- 322
- Citations by year
- 2026: 39 · 2025: 48 · 2024: 73 · 2023: 54 · 2022: 64 · 2021: 75 · 2020: 93 · 2019: 74 · 2018: 66 · 2017: 79 · 2016: 56 · 2015: 48 · 2014: 13
- FWCI
- 7.41
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Cell Death and Disease (publishedVersion, cc-by-nc-nd)
- Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- HAL (submittedVersion, cc-by)
- UCL Discovery (University College London) (submittedVersion)
- Padua Research Archive (University of Padova) (submittedVersion, cc-by-nc-nd)
- Funders
- Association pour la Recherche sur le Cancer
- European Commission
- Agence Nationale de la Recherche
- Ligue Contre le Cancer
- Fondation de France
- Associazione Italiana per la Ricerca sul Cancro
- Institut National Du Cancer
- Laboratoire d'Excellence en Recherche sur le Médicament et l'Innovation Thérapeutique
- Labex Immuno-Oncology
- Topics
- Health Sciences › Medicine › Oncology › Metal complexes synthesis and properties
- Health Sciences › Medicine › Oncology › Drug Transport and Resistance Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cancer therapeutics and mechanisms
- Keywords
- cisplatin resistance, platinum-based chemotherapy, systems biology, chemosensitization, DNA damage response, cellular senescence, mitochondrial apoptosis, adaptive drug resistance, high-content screening, high-throughput screening, cancer chemotherapy
- MeSH terms
- Animals, Antineoplastic Agents, Cisplatin, Humans, Neoplasms, Drug Resistance, Neoplasm, Systems Biology
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.
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