LncRNA MEG3 had anti-cancer effects to suppress pancreatic cancer activity.

Abstract

The aim of this study was to explain the mechanism of lncRNA MEG 3 in pancreatic cancer. We were collecting 30 pancreatic cancer patients, taking the sample from these patients. We measured the PI3K protein expressions from 30 patients by IHC and WB methods and MEG 3 expression by RT-PCR, and analyzed the relationship between PI3K protein expression and pancreatic cancer patients' clinical pathology and the correlation between lncRNA MEG 3 and PI3K. In the cell experiment, PANC-1 cells were divided into three groups: NC, BL and lncRNA groups, after treatment,we measured cell proliferation rate of 3 groups by MTT methods, evaluated cell apoptosis and cell cycle using flow cytometry, tested the invasion cells and migrate rate of 3 groups by transwell and wound healing assays. Compared with carcinoma adjacent tissue, The PI3K protein expression of pancreatic cancer tissue were significantly up-regulation (P>0.05). MEG 3 gene expression was negatively correlated with PI3K expression. The MEG 3 was negatively correlated with tumor size, Metastasis and Vascular invasion in pancreatic cancer (P<0.05, respectively). In the cell experiment, The cell proliferation and apoptosis rates of lncRNA group were significantly difference compared with NC group (P<0.05, respectively), and the G1 phase rate of lncRNA group was higher than NC group (P<0.05). The invasion cells and wound healing rate were significantly reduced in lncRNA group than those in NC group (P<0.05, respectively). MEG 3 over-expressing had anti-cancer effects to suppress pancreatic cancer activity by regulation PI3K/AKT/Bcl-2/Bax/Cyclin D1/P53 and PI3K/AKT/MMP-2/MMP-9 signaling pathways.