Department of General Surgery, Ruijin Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200025, China; Research Institute of Digestive Surgery, Ruijin Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200025, China.
Department of General Surgery, Ruijin Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200025, China; Research Institute of Digestive Surgery, Ruijin Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200025, China.
Biomed Pharmacother. 2017 May;89:1269-1276. doi: 10.1016/j.biopha.2017.02.041. Epub 2017 Mar 17.
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.
本研究旨在解释长链非编码 RNA MEG3 在胰腺癌中的作用机制。
我们收集了 30 名胰腺癌患者的样本，通过免疫组化（IHC）和 Western blot（WB）方法测量 30 名患者的 PI3K 蛋白表达，通过 RT-PCR 测量 MEG3 表达，并分析 PI3K 蛋白表达与胰腺癌患者临床病理的关系以及长链非编码 RNA MEG3 与 PI3K 的相关性。在细胞实验中，将 PANC-1 细胞分为三组：NC 组、BL 组和 lncRNA 组，用 MTT 法测量三组细胞的增殖率，用流式细胞术评估细胞凋亡和细胞周期，用 Transwell 和划痕愈合实验检测三组细胞的侵袭和迁移率。
与癌旁组织相比，胰腺癌组织的 PI3K 蛋白表达明显上调（P>0.05）。MEG3 基因表达与 PI3K 表达呈负相关。MEG3 与胰腺癌的肿瘤大小、转移和血管侵犯呈负相关（P<0.05）。在细胞实验中，lncRNA 组的细胞增殖率和凋亡率与 NC 组相比差异有统计学意义（P<0.05），lncRNA 组的 G1 期比例高于 NC 组（P<0.05）。lncRNA 组的侵袭细胞数和划痕愈合率明显低于 NC 组（P<0.05）。
过表达 MEG3 通过调节 PI3K/AKT/Bcl-2/Bax/Cyclin D1/P53 和 PI3K/AKT/MMP-2/MMP-9 信号通路发挥抗癌作用，抑制胰腺癌活性。
