Sikora Ewa, Bielak-Żmijewska Anna, Mosieniak Grażyna
Instytut Biologii Doświadczalnej PAN im. M. Nenckiego w Warszawie.
Postepy Biochem. 2018 Oct 15;64(2):110-118. doi: 10.18388/pb.2018_120.
Cell senescence is a process that occurs due to telomere erosion or can be induced by various stresses. Senescent cells cease to divide but remain alive, metabolically active and able to secrete many molecules. They also show many hallmarks of senescence, such as enlarged size, increased granularity, increased activity of SA-β-galactosidase, increased level of cyclin-dependent kinase inhibitors, p16 and p21, and DNA damage foci. Originally, cell senescence was attributed to proliferating normal cells, in contrast to cancer cells, which were considered as those endowed with indefinite growth ability. Recently, it has become evident that anticancer treatment induces senescence in cancer cells. Moreover, certain hallmarks of senescence were detected in non-proliferating post-mitotic cells. There are many signalling pathways involved in cell senescence, but the most prevalent is the DNA damage response pathway. In this review we have summarized our long lasting input in the global study of the mechanisms of senescence of normal and cancer cells and discussed the diversity of the concept of cell senescence.
细胞衰老 是一种由于端粒侵蚀而发生的过程，或者可由各种应激诱导产生。衰老细胞停止分裂，但仍存活，具有代谢活性且能够分泌多种分子。它们还表现出许多衰老特征，如体积增大、颗粒度增加、β-半乳糖苷酶活性增加、细胞周期蛋白依赖性激酶抑制剂p16和p21水平升高以及DNA损伤灶。最初，细胞衰老被认为是增殖的正常细胞所特有的，与被认为具有无限生长能力的癌细胞形成对比。最近，有证据表明抗癌治疗可诱导癌细胞衰老。此外，在非增殖的有丝分裂后细胞中也检测到了某些衰老特征。细胞衰老涉及许多信号通路，但最普遍的是DNA损伤反应通路。在本综述中，我们总结了我们在正常细胞和癌细胞衰老机制的全球研究中的长期投入，并讨论了细胞衰老概念的多样性。
