Dissecting epigenetic silencing complexity in the mouse lung cancer suppressor gene Cadm1.

ABSTRACT: Disease-oriented functional analysis of epigenetic factors and their regulatory mechanisms in aberrant silencing is a prerequisite for better diagnostics and therapy. Yet, the precise mechanisms are still unclear and complex, involving the interplay of several effectors including nucleosome positioning, DNA methylation, histone variants and histone modifications. We investigated the epigenetic silencing complexity in the tumor suppressor gene Cadm1 in mouse lung cancer progenitor cell lines, exhibiting promoter hypermethylation associated with transcriptional repression, but mostly unresponsive to demethylating drug treatments. After predicting nucleosome positions and transcription factor binding sites along the Cadm1 promoter, we carried out single-molecule mapping with DNA methyltransfe

SUBMITTER: Reamon-Buettner SM 

PROVIDER: S-EPMC3368868 | biostudies-literature | 2012

REPOSITORIES: biostudies-literature