| Literature DB >> 21637919 |
Yasuko Ochi1, Tokuhiro Chano, Kaichiro Ikebuchi, Hirokazu Inoue, Takahiro Isono, Akihito Arai, Hitosuke Tameno, Taketoshi Shimada, Yasuo Hisa, Hidetoshi Okabe.
Abstract
RB1-inducible coiled-coil 1 (RB1CC1, also known as FIP200) is involved in dephosphorylation and increase of retinoblastoma tumor suppressor protein (RB1), but the RB1CC1 molecular mechanism in the dephosphorylation of RB1 is not fully understood. We determined that RB1CC1 activates the expression of p16 (also called INK4a/CDKN2a) through the activation of its promoter, using chromatin immunoprecipitation (ChIP) and p16 promoter-luciferase reporter assays. In addition, RB1CC1 essentially requires binding with hSNF5 (also known as BAF47/INI1, a chromatin-remodeling factor) to activate the p16 promoter, in order to enhance the RB1 pathway and acts as a tumor suppressor. Evaluation of the RB1CC1 mechanism of action is expected to provide useful information for clinical practice and future therapeutic strategies in human cancers.Entities:
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Year: 2011 PMID： 21637919 DOI： 10.3892/or.2011.1329
Source DB: PubMed Journal: Oncol Rep ISSN： 1021-335X Impact factor: 3.906