| Literature DB >> 27773593 |
Lin Shan1, Xing Zhou1, Xinhua Liu1, Yue Wang1, Dongxue Su1, Yongqiang Hou1, Na Yu1, Chao Yang1, Beibei Liu1, Jie Gao1, Yang Duan1, Jianguo Yang2, Wanjin Li2, Jing Liang2, Luyang Sun2, Kexin Chen3, Chenghao Xuan1, Lei Shi1, Yan Wang1, Yongfeng Shang4.
Abstract
Although clinically associated with severe developmental defects, the biological function of FOXK2 remains poorly explored. Here we report that FOXK2 interacts with transcription corepressor complexes NCoR/SMRT, SIN3A, NuRD, and REST/CoREST to repress a cohort of genes including HIF1β and EZH2 and to regulate several signaling pathways including the hypoxic response. We show that FOXK2 inhibits the proliferation and invasion of breast cancer cells and suppresses the growth and metastasis of breast cancer. Interestingly, FOXK2 is transactivated by ERα and transrepressed via reciprocal successive feedback by HIF1β/EZH2. Significantly, the expression of FOXK2 is progressively lost during breast cancer progression, and low FOXK2 expression is strongly correlated with higher histologic grades, positive lymph nodes, and ERα-/PR-/HER2- status, all indicators of poor prognosis.Entities:
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Year: 2016 PMID： 27773593 DOI： 10.1016/j.ccell.2016.09.010
Source DB: PubMed Journal: Cancer Cell ISSN： 1535-6108 Impact factor: 31.743