406948

MIR15A

PURPOSES: To investigate whether miR-15a inhibits cell proliferation and epithelial-mesenchymal transition (EMT) in pancreatic ductal adenocarcinoma (PDAC) via the down-regulation of B cell-specific moloney murine leukemia virus insertion site 1 (Bmi-1) expression. METHODS AND RESULTS: miR-15a and Bmi-1 expressions in normal pancreatic tissue and PDAC tissue were measured. The relationship between miR-15a and Bmi-1 expression was analyzed. We found that miR-15a suppressed the expression of Bmi-1 and PDAC cell proliferation; E-cadherin expression was visibly up-regulated after silencing Bmi-1 by transfecting miR-15a into PDAC cell line. CONCLUSION: miR-15a inhibits cell proliferation and EMT in PDAC via the down-regulation of Bmi-1 expression.CI - Copyright (c) 2013 Elsevier Ireland Ltd. All rights reserved.

High glucose (HG) has been reported to be associated with renal dysfunction. And one potential mechanism underlining the dysfunction is the epithelial-mesenchymal transition (EMT) of renal tubular epithelial cells. Present study showed that EMT was induced in the HG-treated renal tubular epithelial cells by promoting the expression of mesenchymal phenotype molecules, such as alpha-SMA and collagen I, and down-regulating the expression of epithelial phenotype molecule E-cadherin. Moreover, we have identified the down-regulation of miR-15a which was accompanied with the HG-induced EMT. And the miR-15a overexpression inhibited the alpha-SMA, collagen I expression, and the promotion of E-cadherin expression by targeting and down-regulating AP4 which was also significantly promoted by the HG in the renal tubular epithelial cells. Thus, this study revealed that the weakening regulation on the AP4 expression by miR-15a might contribute to the HG-induced EMT in the renal tubular epithelial cells.