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Abstract
JUNG HWA KIM1,*, BOGYOU KIM1,*, LING CAI2,*, HEE JUNE CHOI1, KENNETH A. OHGI2, CHRIS TRAN3, CHARLIE CHEN3, CHIN HA CHUNG1, OTMAR HUBER4, DAVID W. ROSE5, CHARLES L. SAWYERS3, MICHAEL G. ROSENFELD2 & SUNG HEE BAEK1
Correspondence and requests for materials should be addressed to S.H.B. or M.G.R..
Defining the molecular strategies that integrate diverse signalling pathways in the expression of specific gene programmes that are critical in homeostasis and disease remains a central issue in biology. This is particularly pertinent in cancer biology because downregulation of tumour metastasis suppressor genes is a common occurrence, and the underlying molecular mechanisms are not well established. Here we report that the downregulation of a metastasis suppressor gene, KAI1, in prostate cancer cells involves the inhibitory actions of -catenin, along with a reptin chromatin remodelling complex. This inhibitory function of -catenin-reptin requires both increased -catenin expression and recruitment of histone deacetylase activity. The coordinated actions of -catenin-reptin components that mediate the repressive state serve to antagonize a Tip60 coactivator complex that is required for activation; the balance of these opposing complexes controls the expression of KAI1 and metastatic potential. The molecular mechanisms underlying the antagonistic regulation of -catenin-reptin and the Tip60 coactivator complexes for the metastasis suppressor gene, KAI1, are likely to be prototypic of a selective downregulation strategy for many genes, including a subset of NF-B target genes.
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