lncRNA GMDS-AS1 restrains lung adenocarcinoma progression via recruiting TAF15 protein to stabilize SIRT1 mRNA

Author:

Peng Wei123ORCID,Jiang Junjie45ORCID,Fu Jia1ORCID,Duan Huaxin123ORCID,Wang Jia6ORCID,Duan Chaojun45ORCID

Affiliation:

1. Department of Oncology, Hunan Provincial People's Hospital, The First Affiliated Hospital of Human Normal University, Changsha, Hunan, 410005, P.R. China

2. Key Laboratory of Study & Discovery of Small Targeted Molecules of Hunan Province, Hunan Normal University, Changsha, Hunan, 410013, P.R. China

3. Laboratory of Oncology, Institute of Translational Medicine, Hunan Provincial People's Hospital, Changsha, Hunan, 410005, P.R. China

4. Institute of Medical Sciences, Xiangya Hospital, Central South University, Xiangya Road 87th, Changsha, Hunan, 410008, P.R. China

5. Key Laboratory of Cancer Proteomics of Chinese Ministry of Health, Xiangya Hospital, Central South University, Xiangya Road 87th, Changsha, Hunan, 410008, P.R. China

6. Hunan Provincial People's Hospital, The First Affiliated Hospital of Human Normal University, Changsha, Hunan, 410005, P.R. China

Abstract

Aim: To explore the roles of GMDS-AS1 in the epithelial–mesenchymal transition (EMT) of lung adenocarcinoma (LUAD). Materials & methods: Cell functions were detected by flow cytometry, cell counting kit-8, wound healing assays and transwell assays. RNA immunoprecipitation and pull-down assays were applied for determining the interaction among GMDA-AS1, TAF15 and SIRT1. A subcutaneous xenograft model was established. Results: GMDS-AS1 downregulation was associated with poor survival of LUAD patients. GMDS-AS1 repressed malignant phenotypes, tumor growth and EMT in vitro and in vivo. Mechanically, GMDS-AS1 recruited TAF15 protein to stabilize SIRT1 mRNA and thereby deacetylated p65 and reduced the recruitment of p65 to MMP-9 promoter, thus inhibiting MMP-9 expression. Conclusion: GMDS-AS1 represses EMT by recruiting TAF15 protein to stabilize SIRT1 mRNA and deacetylate p65, thus restraining LUAD progression.

Funder

Outstanding Youth Program of Hunan Provincial Department of Education

Changsha Natural Science Foundation

Hunan Natural Science Foundation

National Natural Science Foundation of China

Publisher

Future Medicine Ltd

Subject

Cancer Research,Genetics

全球学者库

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

"全球学者库"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,当前全球学者库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 © 2019-2023 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