Inhibition Sequence of miR-205 Hinders the Cell Proliferation and Migration of Lung Cancer Cells by Regulating PETN-Mediated PI3K/AKT Signal Pathway.

Abstract

The aim of this study was to identify the pro-tumor role of miR-205 in patients with lung cancer (LC) on the cell proliferation and migration through regulating PTEN-mediated PI3K/AKT signal pathway. Paired cancer tissues and adjacent tissues were collected from 107 LC patients who received treatment in Jinan Central hospital. In addition, the purchased LC cell lines were transfected into HCC827 cell line to observe and compare the biological behaviors. Compared with adjacent tissues, miR-205 was statistically higher in LC tissues, while PTEN was notably lower (P < 0.05). Inhibition of miR-205 not only suppressed cell proliferation, migration and invasion, increased apoptosis rate, but regulated epithelial mesenchymal transformation (EMT)-related proteins. Likewise, overexpression of PETN played the same role as that of miR-205 inhibition sequence. Inhibited miR-205 or PTEN overexpression brought dramatically decreased PI3K and p-Akt. The relationship between miR-205 and PTEN was verified through the biological prediction website and luciferase reporter. Co-transfection experiments revealed that after cotransfection of miR-205 inhibitor and si-PETN, the cell proliferation and invasion showed no marked difference between cotransfection group and NC group. MiR-205 is involved in LC cell proliferation and migration by regulating PETN-mediated PI3K/AKT signal pathway, which may be a feasible treatment target for LC in clinical practice.