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YTHDC1 Regulates m6A-Dependent TERT mRNA Stability to Modulates Ovarian Cancer Senescence

GSE306807 Homo sapiens Expression profiling by high throughput sequencing 6 samples Submitted 2025/11/01 Platform GPL30209
Summary
The m6A reader protein YTHDC1 is implicated in the pathogenesis of diverse cancer types. In this study, we identify YTHDC1 as a critical regulator of senescence in ovarian cancer cells. We demonstrate that knockdown of YTHDC1 inhibits cell proliferation and promotes cellular senescence.Mechanistically, depleting YTHDC1 diminishes the stability of TERT mRNA in an m6A-dependent manner, thereby reducing TERT expression at both the mRNA and protein levels. This reduction leads to decreased telomerase activity, ultimately triggering senescence. Notably, the senescence phenotype induced by YTHDC1 knockdown can be rescued by the exogenous expression of TERT.
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Also filed as BioProject PRJNA1311810 and SRA study SRP613824. Searching any of these in the dataset finder brings you back here.

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