中文摘要：

细胞衰老是指细胞生长永久阻滞于细胞周期的GI期，出现形态、生化及表观遗传的变化特性．细胞衰老由端粒缩短、DNA损伤、缺氧或癌基因失调等因素引起，它是抵抗肿瘤发生的主要壁垒．原癌基因c-myc编码转录因子，可调控很多基因，进而影响细胞周期演进、衰老、凋亡、代谢等生物学过程-c-Myc蛋白与细胞衰老密切相关，它可影响hTERT、p16、p53、Bmi-1和p27等衰老相关基因转录-c-Myc不仅可抑制复制性衰老，也能抑制癌基因诱发的衰老．c—Myc抑制ras诱导的细胞衰老取决于CDK2-c-Myc失活不仅能够诱导非恶性细胞（如人成纤维细胞）衰老，而且在许多肿瘤细胞中也可诱导衰老．然而，与ras基因类似，在特定条件下，c-Myc也可诱导细胞衰老，并可促进维氏综合症（Wemer syndrome，WRNl缺失细胞的衰老．

英文摘要：

Cellular senescence is a terminal growth arrest in the G1 phase of the cell cycle, featuring characteristic morphological, biochemical, and epigenetical changes. Cellular senescence results from telomere erosion, DNA damage, hypoxia, or oncogene deregulation, and it is one of main barriers of tumorigenesis. Proto-oncogene c-Myc encodes a transcription factor that can regulate the transcription of many genes, thereby affects different biological processes such as the cell cycle progression, senescence, apoptosis, metabolism, and so on. The c-Myc protein is closely related to cellular senescence, and it has abilities to affect cellular senescence-associated genes （hTERT, p16, p53, Bmi-1 and p27） transcription. The activation of c-Myc not only inhibits replicative senescence, but also can inhibit oncogene-induced senescence. The c-Myc suppresses Ras-induced cellular senescence with help with CDK2. The inactivation of c-Myc induces senescence in untransformed cells（such as human fibroblasts） as well as in many tumor cells. However, similar to ras gene, under certain conditions, c-Myc can induce cell senescence, and contributes to WRN gene-deficient cells senescence.