Sp1 is involved in the transcriptional activation of p16(INK4) by p21(Waf1) in HeLa cells.
Both p16(INK4) and p21(Waf1) are very important negative regulators of the cell cycle. In this study we examined the effects of p21(Waf1) on the transcription of p16(INK4). We determined that p21(Waf1) can activate the transcription of p16(INK4), and that this effect is GC-box dependent. We also found that the transcription factor Sp1 plays a key role in this event. Upregulation of Sp1 contributes to the transcriptional activation and protein level of p16(INK4) mediated by p21(Waf1), and is a potential point of cooperation between the p16/pRb and p14 (ARF)/p53 tumor suppressor pathways.
Xue
Lixiang
L
Department of Biochemistry and Molecular Biology, Health Science Center, Peking University, 38 Xueyuan Road, Beijing 100083, PR China.
Wu
Junfeng
J
Zheng
Wenjie
W
Wang
Peichang
P
Li
Jun
J
Zhang
Zongyu
Z
Tong
Tanjun
T
D019941:Cyclin-Dependent Kinase Inhibitor p16 / Q000096:biosynthesis* / Q000235:genetics; D050759:Cyclin-Dependent Kinase Inhibitor p21; D016213:Cyclins / Q000235:genetics* / Q000502:physiology; D006367:HeLa Cells; D006801:Humans; D009154:Mutation; D011401:Promoter Regions, Genetic / Q000235:genetics; D016329:Sp1 Transcription Factor / Q000235:genetics* / Q000502:physiology; D015533:Transcriptional Activation; D014162:Transfection; D025803:Tumor Suppressor Protein p14ARF; D015854:Up-Regulation
C493956:CDKN1A protein, human; D019941:Cyclin-Dependent Kinase Inhibitor p16; D050759:Cyclin-Dependent Kinase Inhibitor p21; D016213:Cyclins; D016329:Sp1 Transcription Factor; D025803:Tumor Suppressor Protein p14ARF