miR-153 Overexpression and BCL2 Targeting Induce Apoptosis and Autophagy in HepG2 Cells
摘要
Evidence suggests that downregulation of miR-153 in hepatocellular carcinoma (HCC) cells and tissues promotes cell proliferation. One of the characteristics of cancer cells is the high expression of B-cell lymphoma 2 (BCL2) gene inside the cells, which is a barrier to cell apoptosis. In this study, cloned miR-153 transfection into the HepG2 cancer cells altered the expression of genes associated with autophagy, reduced the BCL2 gene expression, and resulted in apoptosis, as assessed by real-time PCR. The BCL2 gene expression decreased significantly, P < 0.01, in the miR-153-transfected cells, compared to the negative control and empty vector-transfected cells. This analysis was performed using real-time PCR, and its comparison was evaluated using Prism software. This reduction disrupted the Beclin 1 and BCL2 complexes as a type of signal to initiate the process. Also, the expression of light chain 3 and BECN1 genes increased as autophagic genes. The cloning of miR-153 in the PLKO1 vector was found and to be effective, and the expression of miR-153 was confirmed inside the target cells. By targeting the BCL2 gene, reducing its expression, and increasing the expression of LC3 and BECN1 genes in cancer cells, miR-153 might cause apoptosis and autophagy within the HCC cell line. The luciferase assay was used for gene targeting and results was analyzed by ANOVA.