中文摘要：

背景 p16INK4 和 p21Waf1 是有在细胞的老朽的规定的类似的生物功能的肿瘤 suppressors。以前的报告证明 p16INK4 能被 p21Waf1 在 HeLa 房间通过 transcriptional 因素 Sp1 激活。这研究被承担在人的双成纤维细胞 2BS 房间是的 p21Waf1.Methods 的表示和功能上决定 p16INK4 的效果稳定地有感觉( 2BS/p16INK4 )的 transfected ， antisense p16INK4 ( 2BS/asp16INK4 )或空向量( 2BS/neo )他们是的 .Then 由反向抄写的聚合酶链反应( RT-PCR )的 assayed ，荧光激活排序的房间( FACS )，西方的 blot.Results 2BS/p16INK4 房间在 G1 和 G2/M 阶段展出了房间周期拘捕。在 2BS/p16INK4 房间双重的增加，然而并非在 2BS/asp16INK4 房间减少了的内长的 p21Waf1 蛋白质层次。p21Waf1 mRNA 层次没在两 2BS/p16INK4 被影响也不 2BS/asp16INK4 cells.Conclusion p16INK4 可以由 modulating 在细胞的老朽的规定起一个重要作用经由 posttranscriptional 机制的 p21Waf1protein 水平。

英文摘要：

Background Both p16^INK4 and p21waf1 are tumor suppressors with similar biological functions in the regulation of cellular senescence. Previous reports showed that p16^INK4 could be activated by p21waf1 through transcriptional factor Spl in HeLa cells. This study was undertaken to determine the effects of p16^INK4 on the expression and functions of p21^waf1. Methods Human diploid fibroblast 2BS cells were stably transfected with sense （2BS/p16^INK4）, antisense p16^INK4 （2BS/asp16^INK4） or empty vector （2BS/neo） .Then they were assayed by reverse-transcription polymerase chain reaction （RT-PCR）, fluorescence activated cell sorting （FACS） and Western blot. Results 2BS/p16^INK4 cells exhibited cell cycle arrest in both G1 and G2/M phases. Endogenous p21^waf1 protein levels increased twofold in the 2BS/p16^INK4 cells, but not decreased in the 2BS/asp16^INK4 cells. P21^waf1 mRNA levels were not affected in neither 2BS/p16^INK4 nor 2BS/asp16^INK4 cells. Conclusion p16^INK4 may play an important role in the regulation of cellular senescence by modulating the p21^waf1 protein level via the posttranscriptional mechanism.