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Unraveling the enigmatic complexities of BRMS1‐mediated metastasis suppression
Author(s) -
Hurst Douglas R.,
Welch Danny R.
Publication year - 2011
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2011.07.045
Subject(s) - metastasis , epigenetics , biology , microrna , chromatin , cancer research , context (archaeology) , transcription factor , regulation of gene expression , tumor progression , chromatin remodeling , gene , microbiology and biotechnology , cancer , genetics , paleontology
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.