The expression of p21 is upregulated by forkhead box A1/2 in p53-null H1299 cells.
The expression of the cell cycle inhibitor p21 is increased in response to various stimuli and stress signals through p53-dependent and independent pathways. We demonstrate in this study that forkhead box A1/2 (FOXA1/2) is a crucial transcription factor in the activation of p21 transcription via direct binding to the p21 promoter in p53-null H1299 lung carcinoma cells. In addition, histone deacetylase inhibitor trichostatin A (TSA)-mediated upregulation of p21 expression was repressed by knockdown of FOXA1/2 in H1299 cells. Consequently, these results suggest that FOXA1/2 is required for p53-independent p21 expression.
['An|Joo-Hee|JH|', 'Jang|Sang-Min|SM|', 'Kim|Jung-Woong|JW|', 'Kim|Chul-Hong|CH|', 'Song|Peter I|PI|', 'Choi|Kyung-Hee|KH|']
D001483:Base Sequence D045744:Cell Line, Tumor D050759:Cyclin-Dependent Kinase Inhibitor p21 D017353:Gene Deletion D051541:Hepatocyte Nuclear Factor 3-alpha D051542:Hepatocyte Nuclear Factor 3-beta D006801:Humans D006877:Hydroxamic Acids D008969:Molecular Sequence Data D011401:Promoter Regions, Genetic D014158:Transcription, Genetic D015533:Transcriptional Activation D016159:Tumor Suppressor Protein p53 D015854:Up-Regulation
p21 Trichostatin A Target gene Transcription factor FOXA1/2 p53-Independent pathway