miR-200c regulates the translocation of β-catenin from the cytoplasm to the nucleus via inhibition of bromodomain-containing 7 (BRD7, a validated target of miR-200c), a potential tumor-suppressor gene, resulting in increased expression of its transcriptional target genes, cyclin D1 and c-myc, suggesting its potential role for the EC treatment. The gene discussed is CCND1; the disease is neoplasm.