中国科技核心期刊
CN:31-1600/Q
ISSN:1004-0374
“健康与疾病的免疫”国际学术研讨会通知      关于有网站冒充本刊网站的声明
《生命科学》 2008, 20(3): 447-
细胞衰老与肿瘤发生
胡 兵*,安红梅,沈克平
(上海中医药大学附属龙华医院,上海200032)
摘 要:细胞衰老(cell senescence)是指细胞在信号转导作用下不可逆地脱离细胞周期并丧失增殖能力后进入的一种相对稳定的状态。细胞衰老有增殖衰老与早熟衰老两种形式:增殖衰老由端粒缩短激发的信号转导激发,与TP53/CDKN1a (p21WAF-1/Cip1)/pRB/E2F信号通路密切相关;早熟衰老由细胞内在或外在急慢性应激信号引发,与TP53/CDKN1a (p21WAF-1/Cip1)/pRB/E2F或CDKN2a(p16ink4A) /pRB/E2F信号通路相关。目前研究已经证实早熟衰老是细胞在癌变过程中的天然屏障,是继DNA修复、细胞凋亡后的第三大细胞内在抗癌机制,在机体防止肿瘤形成中起重要作用。
关键词:细胞衰老;肿瘤发生;生殖衰老;早熟衰老
中图分类号:Q255;R730.231  文献标识码:A
 
Cellular senescence and carcinogenesis
HU Bing*, AN Hong-mei, SHEN Ke-ping
(Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 200032, China)
Abstract: Cellular senescence, irreversible cell cycle arrest and proliferation ability lost, reflects safeguard machinery that limits the proliferative capacity of the cell exposed to endogenous or exogenous stress signals. Two forms of cell senescence have been found in present, which is replicative senescence and premature senescence. Replicative senescence is initiated by the shortening of telomeres, and related to TP53/CDKN1a (p21WAF-1/Cip1)/pRB/E2F signal pathway. Premature senescence is initiated by endogenous or exogenous acute and chronic stress signals, and related to TP53/CDKN1a (p21WAF-1/Cip1)/pRB/E2F or CDKN2a(p16ink4A) /pRB/E2F pathway. Premature cellular senescence may act in response to oncogenic activation as a natural barrier to interrupt tumorigenesis at a premalignant level. Cellular senescence is a third pathway of reaction of cells to DNA damage in addition to DNA repair/recovery and cell apoptosis from the damage.
Key words: cell senescence; carcinogenesis; replicative senescence; premature senescence
 
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