期刊
JOURNAL OF BIOLOGICAL CHEMISTRY
卷 287, 期 8, 页码 5379-5389出版社
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
DOI: 10.1074/jbc.M111.304287
关键词
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资金
- National Institutes of Health/NINDS [1K08NS051477]
- Centre National de la Recherche Scientifique (CNRS)
- Pasteur Institute of Lille
- Ligue Nationale contre le Cancer (Comite Interregional du Septentrion)
- Association for International Cancer Research (AICR)
- Association pour la Recherche contre le Cancer (ARC) [ARC 3983, ARC 1081]
- CNRS/Region Nord-Pas de Calais
The transcriptional repressor HIC1 (Hypermethylated in Cancer 1) is a tumor suppressor gene inactivated in many human cancers including breast carcinomas. In this study, we show that HIC1 is a direct transcriptional repressor of beta-2 adrenergic receptor (ADRB2). Through promoter luciferase activity, chromatin immunoprecipitation (ChIP) and sequential ChIP experiments, we demonstrate that ADRB2 is a direct target gene of HIC1, endogenously in WI-38 cells and following HIC1 re-expression in breast cancer cells. Agonist-mediated stimulation of ADRB2 increases the migration and invasion of highly malignant MDA-MB-231 breast cancer cells but these effects are abolished following HIC1 re-expression or specific down-regulation of ADRB2 by siRNA treatment. Our results suggest that early inactivation of HIC1 in breast carcinomas could predispose to stress-induced metastasis through up-regulation of the beta-2 adrenergic receptor.
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