To explore the roles of GMDS-AS1 in the epithelial-mesenchymal transition (EMT) of lung adenocarcinoma (LUAD). 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 . A subcutaneous xenograft model was established. GMDS-AS1 downregulation was associated with poor survival of LUAD patients. GMDS-AS1 repressed malignant phenotypes, tumor growth and EMT and . Mechanically, GMDS-AS1 recruited TAF15 protein to stabilize mRNA and thereby deacetylated p65 and reduced the recruitment of p65 to promoter, thus inhibiting MMP-9 expression. GMDS-AS1 represses EMT by recruiting TAF15 protein to stabilize mRNA and deacetylate p65, thus restraining LUAD progression.
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