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 transc...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.展开更多
基金grants from the National Basic Research Program of China(No.2007CB507400)National Nature Science Foundation of China(No.30671064).
文摘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.
