Background:Long non-coding RNA VIM-antisense 1 (VIM-AS1) has been reported that it is involved in the progression of several cancers. However, the aberrant expression profile, clinical significance, and biological function of VIM-AS1in lung adenocarcinoma (LUAD) have not been fully described. We tend to perform a comprehensive analysis to identify the clinical prognostic value of VIM-AS1 for LUAD patients and explore its potential molecular mechanisms in LUAD development.Methods: The expression features of VIM-AS1 in LUAD were identified based on Cancer Genome Atlas database (TCGA) and genotypic tissue expression (GTEx). The LUAD patients' lung tissues were collected to testify above expression features. Survival analysis and COX regression analysis were performed to evaluate the prognostic value of VIM-AS1 in LUAD patients. Then Correlation analysis was performed to filter VIM-AS1 co-expression genes, and their molecular functions were constructed. Furtherly, we constructed the lung carcinoma A549 cell line with VIM-AS1 overexpression to test its effect on cell function.Results: VIM-AS1 expression levels were significantly downregulated in LUAD tissues. VIM-AS1 with low expression is significantly associated with short overall survival (OS), disease-specific survival (DSS), progress free interval (PFI), late T pathological stage, and lymph node metastasis for LUAD patients. The low expression level of VIM-AS1 was an independent risk factor for poor prognosis for LUAD patients. The biological functions of co-expressed genes indicated that VIM-AS1 regulating the apoptosis process may be the potential mechanism for LUAD. Specifically, we testified VIM-AS1 can promote apoptosis in A549 cells.Conclusion: VIM-AS1 was significantly downregulated in LUAD tissues, and it can be a promising prognostic index for LUAD development. VIM-AS1 regulating apoptotic effects may play important roles in LUAD progression.