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FEBS Lett. 2011 Oct 20;585(20):3185-90. doi: 10.1016/j.febslet.2011.07.045. Epub 2011 Aug 5.

Unraveling the enigmatic complexities of BRMS1-mediated metastasis suppression.

Author information

1
Department of Pathology, University of Alabama at Birmingham, Birmingham, AL 35294-0019, USA. DHurst@uab.edu

Abstract

Expression of BRMS1 causes dramatic suppression of metastasis in multiple in vivo model systems. As we gain further insight into the biochemical mechanisms of BRMS1, we appreciate the importance of both molecular and cellular context for functional metastasis suppression. BRMS1 associates with large chromatin remodeling complexes including SIN3:HDAC which are powerful epigenetic regulators of gene expression. Additionally, BRMS1 inhibits the activity of NFκB, a well-known transcription factor that plays significant roles in tumor progression. Moreover, BRMS1 coordinately regulates the expression of metastasis-associated microRNA known as metastamir. How these biochemical mechanisms and biological pathways are linked, either directly or indirectly, and the influence of molecular and cellular context, are critical considerations for the discovery of novel therapeutic targets for the most deadly aspect of tumor progression-metastasis.

PMID:
21827753
PMCID:
PMC3195837
DOI:
10.1016/j.febslet.2011.07.045
[Indexed for MEDLINE]
Free PMC Article

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