Abstract

To investigate the role of miR-150-5p in cell proliferation and apoptosis in human pancreatic cancer cell lines. The expression of miR-150-5p in pancreatic cancer was detected by real time qPCR analysis in 11 pairs of pancreatic cancer tissue and matched adjacent normal tissue samples and in 4 pancreatic cancer cell lines. PANC-1, MIA PaCa-2,BxPC-3 and AsPC-1 cells were transfected with chemically synthesized MiR-150-5p mimics, and CCK-8 assays was then performed to assess cellular functions. To fully understand the mechanisms by which miR-150-5p exerted its function, cell cycle analysis was performed on MIA PaCa-2 and PANC-1 cells 48 hours after transfection, by incubating with propidium iodide (PI)and subsequently analyzed by fluorescence-activated cell sorting (FACS) . Apoptosis assay was performed on MIA PaCa-2 and PANC-1 cell lines 24 hours after transfection using the Annexin V-FITC Apoptosis Detection Kit I (BD Biosciences) and analyzed by FACS. The expression of miR-150-5p was consistently lower in the pancreatic cancer tissues than in normal tissues, and the miR-150-5p was also down-regulated in pancreatic cancer cell lines (P < 0.05) . MiR-150-5p mimics transfection significantly raised the expression level of miR-150-5p mRNA in PANC-1 and MIA PaCa-2 (P < 0.01) . The CCK-8 proliferation assay showed that cell growth was reduced in 4 pancreatic cancer cell lines (AsPC-1, BxPC-3,MIA PaCa-2, PANC-1) of miR-150-5p transfected cells compared with NC-transfected cells. The inhibition rates were 50.7%, 48.6%, 30.8% and 42.3%, respectively (P < 0.01). The apoptotic rate was increased in cells transfected with miR-150-5p mimics (P < 0.01) . The cell cycle analysis in MIA PaCa-2 indicated that miR-150-5p treatment induced cell cycle arrest in G1 phase with a significant increase in the percentage of cells in G1 phase (P < 0.01), and a reduction of the S-phase cell population in MIA PaCa-2 and PANC-1 (P < 0.01). MiR-150-5p is down-regulated in pancreatic cancer. Over-expression of miR-150-5p inhibits cell proliferation, blocked the cell cycle, but promotes cell apoptosis in pancreatic cancer cells.

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