Cancer regulation and the miR-200 cluster has been a family affair for a while now. A new article from a group at The University of Arizona highlights a couple of family members, miR-200c and miR-141, (they must be the attention-starved middle children) and how epigenetic regulation of their expression differs in normal and cancer cells.
Scientists from U of A found correlations in miR-200c/141 expression with cell type, methylation status of the miR-200c/141 Transcription Start Site (TSS), and histone modifications through a series of experiments.
- Methylation of a CpG island near the miR-200c/141 TSS showed strong correlation with miR-200c/141 expression by MassARRAY. Increased methylation = decreased miRNA expression.
- Loss of miR-200c/141 expression is linked to a cancer phenotype, as well as being cell-type and tissue specific.
- Permissive histone marks (H3 acetylation and H3K4 trimetylation) were found in cells with miR-200c/141 expression, while a repressive mark (H3K9 dimethylation) was enriched in non miR-200c/141 expressing cells.
- Use of 5-aza-2’-deoxycitidine restarts miR-200c/141 expression, showing DNA methylation is involved in their transcriptional regulation.
Learn more about the miR-200 family tree at PLoS One, January 2010