Effects of miR-143 overexpression on proliferation, apoptosis, EGFR and downstream signaling pathways in PC9/GR cell line.

OBJECTIVE: The functions of microRNAs in the regulation of apoptosis in non small cell lung cancer (NSCLC) and the application in the therapeutical treatments were intensively studied. However, whether overexpression of miR-143 in lung cancer cells will affect the cell behaviors, such as proliferation or some underlying pathway, is largely unknown. This study aimed to examine the effect of miR-143 in PC9/GR cell line on the proliferation, apoptosis, EGFR and downstream signal pathways. MATERIALS AND METHODS: The non-small cell lung cancer (PC9/GR) cells were treated with concentration-increased gefitinib to acquire gefitinib resistance. Then, the acquired gefitinib-resistance cells were divided into 3 groups, blank control group (BC group), negative control group (NC group), and miR-143 transfected group (miR-143 group). miR-143 mRNA was detected by quantitative PCR. The proliferation was detected by CCK-8. The cell apoptosis was determined by flow cytometry. The expression of EGFR and downstream signal pathway factors of p-EGFR, AKT, p-AKT, ERK1/2 and p-ERK1/2 were detected by Western blot. RESULTS: The cell proliferation in miR-143 transfected group was significantly suppressed compared with BC and NC group, whiletheapoptosis was dramatically increased. The p-EGFR, p-AKT, p-ERK1/2 protein expression was significantly inhibited. CONCLUSIONS: These results demonstrated that overexpression of miR-143 downregulated cell proliferation, promoted the apoptosis, and suppressed the phosphorylation of EGFR, AKT and ERK1/2; thus, miR-143 may play a role in treatment of NSCLC to enhance therapeutic efficacy.