细胞衰老与肿瘤

Cellar Senescence and Tumor

衰老是细胞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,是正常细胞的必然归宿。研究表明,随着细胞衰老,许多基因的表达发生变化,这包括激活因子的抑制和生长抑制因子的过表达,以及下游途径的干预;同时端粒和端粒酶也发生改变。目前的研究结果还表明,衰老与肿瘤的发生和诊治存在密切关系。除对纤维原细胞开展研究外,还涉及到更多类型的细胞,这为更好地确定细胞衰老在肿瘤发生中的作用提供理论基础,同时也可能为肿瘤的抑制提供一个新思路。

Cells withdrawing from the cell cycle and entering the terminally n on-dividing state are referred senescence. With few exceptions, normal cells ne cessarily enter this process. Molecular analyses have identified some changes in gene expressions as cells become senescent, including repression of positive-a cting transcriptional regulators, over-expression of CDK inhibitor, and interfe rence with downstream pathways, and changes in telomere and telomerase. Current findings show that senescence is well connected with tumorigenesis and tumor the rapy. Studies with cell types other than fibroblast will better define the roles of cellar senescence in tumorigenesis, moreover, it may provide a novel therape utic approach to tumor repression.