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The following is a summary of “Epigenetic regulation of diverse cell death modalities in cancer: a focus on pyroptosis, ferroptosis, cuproptosis, and disulfidptosis,” published in the April 2024 issue of Hematology by Zhou et al.
Tumor formation arises from the local hyperplasia of tissues due to the malignant transformation of normal cells under the influence of various physical, chemical, and biological factors. Understanding the mechanisms underlying tumorigenesis is paramount for early prevention and effective treatment strategies. Epigenetic modifications represent a fundamental and intricate aspect of cellular regulation, encompassing DNA methylation, histone modification, non-coding RNA modification, and m6A modification. While programmed cell death traditionally follows a defined pathway governed by cell death-related genes, recent investigations have unveiled novel modes of cell demise, including pyroptosis, ferroptosis, cuproptosis, and disulfideptosis.
Epigenetic modulation of these diverse cell death modalities predominantly involves the regulation of key cell death proteins, exerting influence by either upregulating or downregulating the expression levels of critical proteins. The primary objective of this study is to probe the intricate mechanisms through which epigenetic modifications regulate pyroptosis, ferroptosis, cuproptosis, and disulfideptosis in tumor cells. By adopting a microscopic perspective, the researchers aim to unravel potential triggering factors implicated in tumor development, offering insights into prospective therapeutic targets and novel avenues for designing antitumor drugs or combination therapies.
Source: jhoonline.biomedcentral.com/articles/10.1186/s13045-024-01545-6