The Role of Long Non-Coding RNA LINC00467 in Gastric Carcinoma: High Proliferation, Migration and Autophagy

Author:

Wu Jinhui1,Liu Yang2,Pang Yanchao3,Sun Xiaohong4,Sun Xiaofei1

Affiliation:

1. Department of Gastrointestinal Surgery, Yantai Yuhuangding Hospital, Yantai, 264000, China

2. Department of Laboratory Medicine, Yantai Yuhuangding Hospital, Yantai, 264000, China

3. Department of Intestine Surgery, Yantai Yuhuangding Hospital, Yantai, 264000, China

4. Office of Academic Affairs, Binzhou Medical University, Binzhou, 256600, China

Abstract

The goal of this study is to investigate the role of long non-coding RNA LINC00467 in gastric carcinoma (GC) progression. Differential expressions of LINC00467 in GC samples were detected. By analyzing the follow-up data of recruited GC patients, the influence of LINC00467 on their prognosis was assessed. After knockdown of LINC00467 in SGC7901 and MKN45 cells, cell autophagy was examined by GFP-LC3 puncta assay and Western blot analyses on autophagy-associated genes. Additionally, cell growth and migration were assessed using cell counting kit-8 (CCK-8), 5-ethynyl-2′-deoxyuridine (EdU), and transwell assays. The connection between LINC00467 and miR-18a-5p was studied through a luciferase assay and Pearson correlation analysis. Increased expression of LINC00467 was observed in GC samples and its elevated levels predicted a poor outcome for GC patients. The suppression of LINC00467 reduced the proliferative and migratory capacities of SGC7901 and MKN45 cells. LINC00467 level was closely linked to autophagy activity in GC. The level of miR-18a-5p was decreased in GC tissues and had an inverse correlation with LINC00467, which was established as the target of miR-18a-5p. Upregulated LINC00467 induces growth, metastasis and autophagy activity in GC through negatively regulating miR-18a-5p level, thus leading to the poor prognosis in GC patients.

Publisher

American Scientific Publishers

Subject

Pharmaceutical Science,General Materials Science,Biomedical Engineering,Medicine (miscellaneous),Bioengineering

同舟云学术

1.学者识别学者识别

2.学术分析学术分析

3.人才评估人才评估

"同舟云学术"是以全球学者为主线,采集、加工和组织学术论文而形成的新型学术文献查询和分析系统,可以对全球学者进行文献检索和人才价值评估。用户可以通过关注某些学科领域的顶尖人物而持续追踪该领域的学科进展和研究前沿。经过近期的数据扩容,当前同舟云学术共收录了国内外主流学术期刊6万余种,收集的期刊论文及会议论文总量共计约1.5亿篇,并以每天添加12000余篇中外论文的速度递增。我们也可以为用户提供个性化、定制化的学者数据。欢迎来电咨询!咨询电话:010-8811{复制后删除}0370

www.globalauthorid.com

TOP

Copyright © 2019-2024 北京同舟云网络信息技术有限公司
京公网安备11010802033243号  京ICP备18003416号-3