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Reprogramming the cancer epigenome by “metabolic transduction”
Author(s) -
Byun Jung S,
Gardner Kevin
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.142.8
Subject(s) - chromatin , reprogramming , biology , histone , epigenetics , epigenome , wnt signaling pathway , microbiology and biotechnology , cancer research , signal transduction , gene expression , dna methylation , genetics , cell , gene
C‐terminal binding protein (CtBP) is a dimeric nuclear corepressor complex that functions generally to target chromatin modifying complexes including histone de‐acetylases, histone de‐methlylases, histone methyl‐transferases and DNA methyl‐transferase complexes to chromatin. CtBP thus has the potential to mediate widespread changes in the epigenetic landscape and influence broad programs of cellular behavior. Recently, we showed genome‐wide profiling by ChIP‐seq that CtBP controls a network of genes linked to cellular programs that influence cellular re‐programing or “plasticity” including stem cell transcriptional programs, angiogenesis, and epithelial‐to‐mesenchymal transition. In human breast cancer samples, we find that CtBP protein expression profiling by immunohistochemistry followed by digital quantitation reveals a clear trend between CtBP expression and poor survival from breast cancer. Follow‐up studies show that CtBP RNA are significanlty higher in the endometrial cancer cell line HEC‐1A compared to MCF‐7 and that, similar to breast cancer, central targets of CtBP repression lead to increased signaling through the WNT pathway. This suggested that CtBP may be a common feature in tissues and cellular systems that undergo reprogramming of any type and this capacity to reprogram may be exploited in different epithelial cancer in processes linked to CtBP.