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The expression of p21 is upregulated by forkhead box A1/2 in p53‐null H1299 cells
Author(s) -
An Joo-Hee,
Jang Sang-Min,
Kim Jung-Woong,
Kim Chul-Hong,
Song Peter I.,
Choi Kyung-Hee
Publication year - 2014
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2014.09.033
Subject(s) - trichostatin a , foxa1 , gene knockdown , downregulation and upregulation , transcription factor , histone deacetylase inhibitor , cancer research , histone deacetylase , forkhead transcription factors , chemistry , foxa2 , microbiology and biotechnology , histone , biology , apoptosis , gene , biochemistry
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.