The expression of p21 is upregulated by forkhead box A1/2 in p53-null H1299 cells |
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Authors: | Joo-Hee An Sang-Min Jang Jung-Woong Kim Chul-Hong Kim Peter I. Song Kyung-Hee Choi |
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Affiliation: | 1. Department of Life Science, College of Natural Sciences, Chung-Ang University, Seoul 156-756, Republic of Korea;2. Neurobiology-Neurodegeneration and Repair Laboratory, NEI, National Institutes of Health, Bethesda, MD 20892, USA;3. Department of Dermatology, University of Colorado Denver Anschutz Medical Campus, Aurora, CO 80045, USA |
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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. |
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Keywords: | TSA, trichostatin A FOXA1/2, forkhead box A1/2 FRE, FOXA1/2 responsible element DBD, DNA-binding domain |
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