Inhibitory role of TGIF in the As2O3-regulated p21 WAF1/CIP1 expression

Journal of Biomedical Science
Zi-Miao Liu, Huei-Sheng Huang

Abstract

Although arsenic is an infamous carcinogen, it has been effectively used to treat acute promyelocytic leukemia, and can induce cell cycle arrest or apoptosis in human solid tumors. Previously, we had demonstrated that opposing effects of ERK1/2 and JNK on p21 expression in response to arsenic trioxide (As(2)O(3)) are mediated through the Sp1 responsive elements of the p21 promoter in A431 cells. Presently, we demonstrate that Sp1, and c-Jun functionally cooperate to activate p21 promoter expression through Sp1 binding sites (-84/-64) by using DNA affinity binding, chromatin immunoprecipitation, and promoter assays. Surprisingly, As(2)O(3)-induced c-Jun(Ser63/73) phosphorylation can recruit TGIF/HDAC1 to the Sp1 binding sites and then suppress p21 promoter activation. We suggest that, after As(2)O(3 )treatment, the N-terminal domain of c-Jun phosphorylation by JNK recruits TGIF/HDAC1 to the Sp1 sites and then represses p21 expression. That is, TGIF is involved in As(2)O(3)-inhibited p21 expression, and then blocks the cell cycle arrest.

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Citations

Mar 19, 2013·Developmental and Comparative Immunology·Stephen S WanyonyiKevin R Nicholas
Feb 1, 2011·Toxicological Sciences : an Official Journal of the Society of Toxicology·Huei-Sheng HuangYa-Ling Cheng
Jul 11, 2012·Molecular and Cellular Biology·Nate P HoverterMarian L Waterman
Oct 27, 2016·Tumour Biology : the Journal of the International Society for Oncodevelopmental Biology and Medicine·Yadong WangHaiyan Yang
Oct 17, 2014·Journal of Neurochemistry·Chung-Ching ChioHuei-Sheng Huang

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