Volume 10,Issue 4
The Mechanism and Advances of m6A RNA Methylation in Regulating Cuproptosis in Gastric Cancer
Gastric cancer remains one of the leading causes of cancer-related deaths worldwide, with treatment challenges such as drug resistance and metastasis necessitating novel therapeutic strategies. Cuproptosis, a novel form of regulated cell death first elucidated in 2022, is a copper-ion-dependent process originating from mitochondrial metabolic disturbance. Distinct from other known cell death modalities, the regulation of cuproptosis involves various epigenetic modifications. Among these, N6-methyladenosine (m6A), the most abundant internal chemical modification in eukaryotic mRNA, plays a pivotal role in post-transcriptional regulation during cuproptosis. This review begins with the clinical challenges of gastric cancer, systematically discusses the significance of programmed cell death in its treatment, and then delves into the unique molecular mechanisms and complex regulatory networks of cuproptosis. It particularly focuses on analyzing how m6A modification precisely regulates cuproptosis through a "metabolism–epigenetics" crosstalk mechanism. The aim is to provide a new theoretical foundation and potential therapeutic targets for the precise diagnosis, treatment, and drug development in gastric cancer.
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