Abstract
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.
Keywords:
Target gene; Transcription factor FOXA1/2; Trichostatin A; p21; p53-Independent pathway.
Copyright © 2014 Federation of European Biochemical Societies. All rights reserved.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Base Sequence
-
Cell Line, Tumor
-
Cyclin-Dependent Kinase Inhibitor p21 / genetics*
-
Gene Deletion*
-
Hepatocyte Nuclear Factor 3-alpha / metabolism*
-
Hepatocyte Nuclear Factor 3-beta / metabolism*
-
Humans
-
Hydroxamic Acids / pharmacology
-
Molecular Sequence Data
-
Promoter Regions, Genetic / drug effects
-
Promoter Regions, Genetic / genetics
-
Transcription, Genetic / drug effects
-
Transcriptional Activation / drug effects
-
Tumor Suppressor Protein p53 / deficiency*
-
Tumor Suppressor Protein p53 / genetics*
-
Up-Regulation* / drug effects
Substances
-
Cyclin-Dependent Kinase Inhibitor p21
-
FOXA1 protein, human
-
FOXA2 protein, human
-
Hepatocyte Nuclear Factor 3-alpha
-
Hydroxamic Acids
-
Tumor Suppressor Protein p53
-
Hepatocyte Nuclear Factor 3-beta
-
trichostatin A