Telomeres are repetitive DNA sequences at the ends of chromosomes that protect against genomic instability and prevent unwanted DNA damage responses. In most somatic cells, telomeres progressively shorten with each division, limiting cellular lifespan. However, cancer cells bypass this limitation by activating telomerase or the alternative lengthening of telomeres, enabling unchecked proliferation and tumor progression. This review examines the molecular mechanisms underlying telomere maintenance and their intricate relationship with DNA repair pathways. We discuss how telomere-associated proteins regulate genomic stability and explore therapeutic strategies targeting telomerase and alternative lengthening of telomeres. Challenges such as resistance mechanisms and off-target effects are also considered, highlighting the need for precision approaches in telomere-based cancer therapies.
端粒是位于染色体末端的重复DNA序列，具有维持基因组稳定性、防止异常DNA损伤应答的功能。在大多数体细胞中，端粒会随着细胞分裂逐渐缩短，从而限制细胞寿命。然而，癌细胞通过激活端粒酶或替代性端粒延长机制突破这一限制，实现不受控制的增殖与肿瘤进展。本文综述了端粒维持的分子机制及其与DNA修复通路之间的复杂关联，探讨了端粒相关蛋白如何调控基因组稳定性，并分析了针对端粒酶及替代性端粒延长机制的治疗策略。同时，文中对耐药机制和脱靶效应等挑战进行了探讨，强调了基于端粒的癌症疗法需要向精准化方向发展的必要性。
Telomere Maintenance and DNA Repair: A Bidirectional Relationship in Cancer Biology and Therapy
肿瘤(癌症)患者之家