Tehran University of Medical Sciences Iranian Journal of Public Health 2251-6085 49 6 2020 06 08 1138 1147 Xiaochun HOU Department of Oncology, Second People's Hospital of Nantong, Nantong 226001, P.R.China Jian XU Department of Oncology, Second People's Hospital of Nantong, Nantong 226001, P.R.China Pei HU Department of Oncology, Second People's Hospital of Nantong, Nantong 226001, P.R.China 2019 12 27 2020 04 30 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 proliferation 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.   https://ijph.tums.ac.ir/index.php/ijph/article/view/19287 https://ijph.tums.ac.ir/index.php/ijph/article/download/19287/6827