Division of Molecular Biotherapy, Cancer Chemotherapy Center, Japanese Foundation for Cancer Research, Koto-ku, Tokyo 135-8550, Japan.
Cells. 2019 Jan 31;8(2):107. doi: 10.3390/cells8020107.
Telomeres, the protective structures of chromosome ends are gradually shortened by each cell division, eventually leading to senescence or apoptosis. Cancer cells maintain the telomere length for unlimited growth by telomerase reactivation or a recombination-based mechanism. Recent genome-wide analyses have unveiled genetic and epigenetic alterations of the telomere maintenance machinery in cancer. While telomerase inhibition reveals that longer telomeres are more advantageous for cell survival, cancer cells often have paradoxically shorter telomeres compared with those found in the normal tissues. In this review, we summarize the latest knowledge about telomere length alterations in cancer and revisit its rationality. Finally, we discuss the potential utility of telomere length as a prognostic biomarker.
端粒是染色体末端的保护结构，每次细胞分裂都会逐渐缩短，最终导致衰老或凋亡。癌细胞通过端粒酶的重新激活或基于重组的机制来维持端粒长度，从而实现无限生长。最近的全基因组分析揭示了端粒维持机制在癌症中的遗传和表观遗传改变。虽然端粒酶抑制表明较长的端粒更有利于细胞存活，但与正常组织中的端粒相比，癌细胞的端粒通常更短，这是一种矛盾的现象。在这篇综述中，我们总结了关于癌症中端粒长度改变的最新知识，并重新探讨了其合理性。最后，我们讨论了端粒长度作为预后生物标志物的潜在应用。
