Posttranscriptional induction of p21Waf1 mediated by ectopic p16INK4 in human diploid fibroblast.
- Author:
Xiao-lin HAN
1
;
Fu-guo WU
;
Zong-yu ZHANG
;
Tan-jun TONG
Author Information
- Publication Type:Journal Article
- MeSH: Cell Cycle; Cells, Cultured; Cellular Senescence; Cyclin-Dependent Kinase Inhibitor p16; physiology; Cyclin-Dependent Kinase Inhibitor p21; physiology; Fibroblasts; metabolism; Humans; Transcription, Genetic
- From: Chinese Medical Journal 2007;120(5):405-409
- CountryChina
- Language:English
-
Abstract:
BACKGROUNDBoth p16(INK4) and p21(Waf1) are tumor suppressors with similar biological functions in the regulation of cellular senescence. Previous reports showed that p16(INK4) could be activated by p21(Waf1) through transcriptional factor Sp1 in HeLa cells. This study was undertaken to determine the effects of p16(INK4) on the expression and functions of p21(Waf1).
METHODSHuman 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.
RESULTS2BS/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.
CONCLUSIONp16(INK4) may play an important role in the regulation of cellular senescence by modulating the p21(Waf1) protein level via the posttranscriptional mechanism.
