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Review
. 2022 Sep 24;12(10):1365.
doi: 10.3390/biom12101365.

Cisplatin Resistance: Genetic and Epigenetic Factors Involved

Affiliations
Review

Cisplatin Resistance: Genetic and Epigenetic Factors Involved

Yuliannis Lugones et al. Biomolecules. .

Abstract

Cisplatin (CDDP) is the drug of choice against different types of cancer. However, tumor cells can acquire resistance to the damage caused by cisplatin, generating genetic and epigenetic changes that lead to the generation of resistance and the activation of intrinsic resistance mechanisms in cancer cells. Among them, we can find mutations, alternative splicing, epigenetic-driven expression changes, and even post-translational modifications of proteins. However, the molecular mechanisms by which CDDP resistance develops are not clear but are believed to be multi-factorial. This article highlights a description of cisplatin, which includes action mechanism, resistance, and epigenetic factors involved in cisplatin resistance.

Keywords: cancer; cisplatin; drug resistance; epigenetics.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Contribution of NF-κΒ to cisplatin resistance. Cisplatin resistance is caused by downregulation of CYLD lysine 63 deubiquitinase (CYLD), triggering the suppression of cell death via NF-κB hyperactivation. TNF-α also contributed to NF-κΒ activation and cell resistance. Created with Biorender.com.
Figure 2
Figure 2
Mechanisms of resistance to cisplatin. Pre-target resistance related to the control of the entry or exit of cisplatin into the cell; on-target resistance implicates mechanisms involved in DNA damage; post-target resistance includes mechanisms that interfere with cell death caused by DNA adducts; and off-target resistance is related to cisplatin-induced proapoptotic events. Blue circle: cisplatin. Created with Biorender.com (https://biorender.com/, accessed on 1 August 2022).

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