Metastasis suppression by BRMS1 associated with SIN3 chromatin remodeling complexes.
Epigenetic regulation of gene transcription by histone modification and chromatin remodeling has been linked to many biological and pathological events including cancer metastasis. Breast cancer metastasis suppressor 1 (BRMS1) interacts with SIN3 chromatin remodeling complexes, and, upon forced expression in metastatic cells, a nearly complete suppression of metastasis is noted without preventing primary tumor growth. The data for BRMS1-mediated metastasis suppression and SIN3 interaction are clear; however, connecting the inhibition directly to the association of BRMS1 with SIN3 complexes is currently not well defined. Considering the recent advancements in developing epigenetic drugs for cancer therapy, an improved understanding of how the interactions between BRMS1 and SIN3 regulate the process of metastasis should lead to novel therapies specifically targeting the most deadly aspect of tumor progression. In this article, the data for BRMS1-mediated metastasis suppression are reviewed with a focus on how the SIN3 chromatin remodeling complexes may be functionally involved.
Department of Pathology, University of Alabama at Birmingham, 1670 University Blvd., VH-G019, Birmingham, AL 35294-0019, USA. DHurst@uab.edu
Douglas R
DR
Hurst
D000818:Animals; D042002:Chromatin Assembly and Disassembly; D056572:Histone Deacetylase Inhibitors / Q000627:therapeutic use; D006801:Humans; D009362:Neoplasm Metastasis / Q000517:prevention & control*; D009363:Neoplasm Proteins / Q000235:genetics / Q000502:physiology*; D012097:Repressor Proteins; D056264:Sin3 Histone Deacetylase and Corepressor Complex / Q000502:physiology*; D025521:Tumor Suppressor Proteins / Q000502:physiology*
C410024:BRMS1 protein, human; D056572:Histone Deacetylase Inhibitors; D009363:Neoplasm Proteins; D012097:Repressor Proteins; D025521:Tumor Suppressor Proteins; D056264:Sin3 Histone Deacetylase and Corepressor Complex