4.7 Article

lncRNA MEG3 had anti-cancer effects to suppress pancreatic cancer activity

Journal

BIOMEDICINE & PHARMACOTHERAPY
Volume 89, Issue -, Pages 1269-1276

Publisher

ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
DOI: 10.1016/j.biopha.2017.02.041

Keywords

MEG 3; PI3K; AKT; Bcl-2; Bax; Cyclin D1; P53; MMP-2; MMP-9

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Aim: The aim of this study was to explain the mechanism of lncRNA MEG 3 in pancreatic cancer. Methods: 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. Results: 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). Conclusion: MEG 3 over-expressing had anti-cancer effects to suppress pancreatic cancer activity by regulation PI3K/AKT/Bcl-2/Bax/CyclinD1/P53 and PI3K/AKT/MMP-2/MMP-9 signaling pathways. (C) 2017 Elsevier Masson SAS. All rights reserved.

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