细胞衰老与肿瘤发生

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（p21^WAF-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（p21^WAF-1/Cip1）/pRB/E2F或CDKN2a（p16^ink4A）/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。

Cellular senescence and carcinogenesis

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/CDKNla （p21^WAF-1/Cip1）/pRB/E2F signal pathway. Premature senescence is initiated by endogenous or exogenous acute and chronic stress signals, and related to TP53/CDKN 1 a （p21^WAF-1/Cip1）/pRB/E2F or CDKN2a（p16^ink4A）/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.