摘要
细胞衰老是指细胞在外在微环境变化或内在特定基因表达与失活等因素作用下脱离细胞周期并不可逆地丧失增殖能力后进入的一种相对稳定的状态，能够被端粒的变化或不同形式的胁迫所触发。类似于癌基因诱导凋亡，多种不同癌基因也可以引起细胞衰老。细胞衰老依赖的生长停滞主要是通过p53和p16／pRB肿瘤抑制信号通路建立和维持的。从生物学功能方面看，细胞衰老与肿瘤发生及治疗密切相关。基因操作或用化疗药物等处理可以诱导某些肿瘤细胞衰老，阐明这一过程的发生机制有助于癌症治疗策略的发展。对于肿瘤发生过程中的细胞衰老仍为生物学研究领域的热点。
Cellular senescence is broadly defined as the physiological program of terminal growth arrest. Cellular senescence could be triggered by short chromosome telomeres, activated oncogene, as well as cell stress, and mediated by p53 and pl6/pRB tumor suppressor pathways. Treatment- induced senescence, which has both similarit with or difference from replicative senescence of normal cells,was shown to be one of the key determi- nants of tumor response to therapy in vitro and in vivo. Elucidation of the genes and regulatm~~ mechanism which determines different aspects of tumor senescence makes it possible to design new therapeutic approaches for im- proving the efficacy and decreasing the side effect of cancer therapy. The elucidation of the biological aspects of tumor cell senescence offers the plausible approach for the development of novel therapeutic strategies, which may stop the growth of tumor cells.
出处
《实用肿瘤学杂志》
CAS
2013年第2期185-189,共5页
Practical Oncology Journal
