Mechanism of miRNA-26a on the Proliferation of Pancreatic Tumor Cells by Regulating the Expression of Cycline2

Background: qrt-pcr was used to measure the expression of mirna-26a in pancreatic epithelial cells (hpde) and human pancreatic cancer cell lines panc-1 and mia paca-2. methods: panc-1 and mia paca-2 cell lines were infected with lentiviruses to construct panc-mir-26a and mia-mir-26a, and rt-pcr was used to detect the infection efficiency. the cell proliferation ability of panc-mir-26a and mia-mir-26a were examined by cck-8 assay, and apoptosis was detected by flow cytometry. western blotting was used to detect the expressions of cycline2 protein and mitochondria-associated apoptotic proteins. results: mir-26a was expressed in human normal pancreatic epithelial cells (hpde), and not detected in panc-1 and mia paca-2; mir-26a was highly expressed in the cell lines panc-mir-26a and mia-mir-26a infected by the virus particles. the absorbance values of panc-mir-26a and mia-mir-26a were lower than those of nc1 and panc-1 in control group. the apoptosis rates of panc-mir-26a and mia-mir-26a were substantially higher than those of the control group. the overexpression of mir-26a inhibited the expression of the target protein cycline2 in panc-mir-26a and mia-mir-26a. the expression of the anti-apoptotic protein bcl-2 was decreased in panc-mir-26a and mia-mir-26a, while the expression of the pro-apoptotic protein bax was increased. compared with hpde, mir-26a was down-regulated in panc-1 and mia paca-2. after overexpression of mir-26a, the prolifera-tion of panc-1 and mia paca-2 cell lines was weakened. conclusion: molecular mechanism is the negative regulation of cycline2 by mir-26a as well as the expressions of downstream mitochondrial apoptosis proteins bcl-2 and bax.