An Joo-Hee, Jang Sang-Min, Kim Jung-Woong, Kim Chul-Hong, Song Peter I, Choi Kyung-Hee
Department of Life Science, College of Natural Sciences, Chung-Ang University, Seoul 156-756, Republic of Korea.
Department of Life Science, College of Natural Sciences, Chung-Ang University, Seoul 156-756, Republic of Korea; Neurobiology-Neurodegeneration and Repair Laboratory, NEI, National Institutes of Health, Bethesda, MD 20892, USA.
FEBS Lett. 2014 Nov 3;588(21):4065-70. doi: 10.1016/j.febslet.2014.09.033. Epub 2014 Oct 2.
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.
细胞周期抑制剂p21的表达通过p53依赖和非依赖途径响应各种刺激和应激信号而增加。我们在本研究中证明，叉头框A1/2（FOXA1/2）是p53缺失的H1299肺癌细胞中通过直接结合p21启动子激活p21转录的关键转录因子。此外，组蛋白去乙酰化酶抑制剂曲古抑菌素A（TSA）介导的p21表达上调在H1299细胞中被FOXA1/2的敲低所抑制。因此，这些结果表明FOXA1/2是p53非依赖的p21表达所必需的。
