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

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