Dengqiang Liu1, Peng Xiao1, Chao Feng1, Hui Meng2, Enxu Bi1. 1. Department of General Surgery, Qingdao West Coast New Area Central Hospital , Qingdao, Shandong, China. 2. Department of Gynecology, Qingdao West Coast New Area Central Hospital , Qingdao, Shandong, China.
Abstract
Background: Gastric carcinoma (GC) is a common malignant tumor. Recently, it has been found that long non-coding RNAs (lncRNAs) play important role in cancer. In this paper, we investigated the effects and mechanism of lncRNA GASL1 in GC cells. Methods: GASL1 level in GC cells was up-regulated via cell transfection. Cell proliferation, migration, invasion were detected by CCK-8, BrdU, Transwell assays and western blot. In addition, the regulation of GASL1 on microRNA (miR)-106a level was detected using RT-qPCR and the binding between GASL1 and miR-106a was confirmed by bioinformatic prediction and luciferase reporter assay. The effects of overexpressing miR-106a on GASL1-regulated GC cell behaviors were further explored. Moreover, western blot also was used to detect the pathway-related proteins. Results: Overexpression of GASL1 decreased the viability and BrdU levels. Meanwhile, CyclinD1 level was decreased while p53 and p21 levels were strengthened by overexpression of GASL1. On cell metastasis, up-regulation of GASL1 decreased cell migration, invasion and related proteins matrix metalloproteinase (MMP)-9 and Vimentin levels. Meanwhile, silencing GASL1 exerted opposite effects on GC cells. Moreover, GASL1 negatively regulated and targeted miR-106a. Up-regulation of miR-106a weakened the functions of GASL1 in cell proliferation and metastasis. Besides, GASL1 decreased the relate-protein levels of PI3K/AKT and ras/raf/MEK/ERK pathways while miR-106a weakened these changes. ConclusionGASL1 restrained GC cell proliferation and metastasis and blocked PI3K/AKT and ras/raf/MEK/ERK pathways by sponging miR-106a.
Background: Gastric carcinoma (GC) is a common malignant tumor. Recently, it has been found that long non-coding RNAs (lncRNAs) play important role in cancer. In this paper, we investigated the effects and mechanism of lncRNA GASL1 in GC cells. Methods: GASL1 level in GC cells was up-regulated via cell transfection. Cell proliferation, migration, invasion were detected by CCK-8, BrdU, Transwell assays and western blot. In addition, the regulation of GASL1 on microRNA (miR)-106a level was detected using RT-qPCR and the binding between GASL1 and miR-106a was confirmed by bioinformatic prediction and luciferase reporter assay. The effects of overexpressing miR-106a on GASL1-regulated GC cell behaviors were further explored. Moreover, western blot also was used to detect the pathway-related proteins. Results: Overexpression of GASL1 decreased the viability and BrdU levels. Meanwhile, CyclinD1 level was decreased while p53 and p21 levels were strengthened by overexpression of GASL1. On cell metastasis, up-regulation of GASL1 decreased cell migration, invasion and related proteins matrix metalloproteinase (MMP)-9 and Vimentin levels. Meanwhile, silencing GASL1 exerted opposite effects on GC cells. Moreover, GASL1 negatively regulated and targeted miR-106a. Up-regulation of miR-106a weakened the functions of GASL1 in cell proliferation and metastasis. Besides, GASL1 decreased the relate-protein levels of PI3K/AKT and ras/raf/MEK/ERK pathways while miR-106a weakened these changes. ConclusionGASL1 restrained GC cell proliferation and metastasis and blocked PI3K/AKT and ras/raf/MEK/ERK pathways by sponging miR-106a.
Authors: Ismael Riquelme; Oscar Tapia; Jaime A Espinoza; Pamela Leal; Kurt Buchegger; Alejandra Sandoval; Carolina Bizama; Juan Carlos Araya; Richard M Peek; Juan Carlos Roa Journal: Pathol Oncol Res Date: 2016-05-07 Impact factor: 3.201