作者: Tae-Dong Kim , Sook Shin , William L. Berry , Sangphil Oh , Ralf Janknecht
DOI: 10.1002/JCB.24009
关键词: Histone H3 、 Cancer research 、 Cell growth 、 Programmed cell death 、 Downregulation and upregulation 、 Chromatin immunoprecipitation 、 Cell cycle 、 Carcinogenesis 、 Apoptosis 、 Biology
摘要: JMJD2A is a transcriptional cofactor and enzyme that catalyzes demethylation of histone H3 lysines 9 36 overexpressed in human tumors, but its role oncogenesis remains unclear. Here, we show interacts with the tumor suppressor p53 both vitro HCT116 colon cancer cells. Chromatin immunoprecipitation assays demonstrated was recruited together to promoter p21 cell cycle inhibitor upon stimulation DNA damaging agent, adriamycin. Downregulation resulted increased expression pro-apoptotic Puma protein, whereas levels anti-apoptotic Bcl-2 protein were decreased. Furthermore, knock-down led reduced HCT116, DLD-1 HT-29 proliferation, while overexpression enhanced proliferation low serum media. Finally, depletion induced apoptosis cells this effect less pronounced absence p53. Collectively, these data indicate novel survival, which mediates effects p53-dependent -independent ways. may therefore be valid target sensitize chemotherapy-induced death growth suppression.