The nuclear protein YTHDC1 directly binds to m6A-modified TERT mRNA transcripts, stabilizing telomerase expression and preventing telomere shortening in ovarian cancer cells. When YTHDC1 was knocked down, cancer cells underwent senescence with dysfunctional telomerase and accelerated telomere erosion. Restoring TERT expression reversed these aging effects, confirming the YTHDC1-telomerase pathway. This discovery reveals a sophisticated molecular hijacking where cancer exploits RNA modification machinery to maintain immortality. The finding bridges two major aging research areas: epitranscriptomics and telomere biology. While telomerase reactivation is a hallmark cancer strategy, the m6A modification angle represents a novel therapeutic vulnerability. YTHDC1-depleted senescent cells showed enhanced sensitivity to the senolytic drug ABT-263, suggesting combination approaches. For longevity research, this work illuminates how cells naturally regulate telomerase through RNA modifications—mechanisms that decline with age. The specificity of YTHDC1 for m6A-marked TERT transcripts suggests targeted interventions might selectively eliminate cancer cells while preserving normal telomerase function in stem cells. However, this remains ovarian cancer-specific research requiring validation across cancer types and normal aging contexts.