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. 2023 May 15;14(8):1417-1426.
doi: 10.7150/jca.83639. eCollection 2023.

lncRNA VIM-AS1 acts as a prognostic biomarker and promotes apoptosis in lung adenocarcinoma

Jianhong Kang  1 , Maimaiti Abudurufu  1 , Shuwei Zhang  2 , Wei Jiang  3 , Honghe Luo  1
Affiliations

lncRNA VIM-AS1 acts as a prognostic biomarker and promotes apoptosis in lung adenocarcinoma

Jianhong Kang et al. J Cancer. .

Abstract

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.

Keywords: VIM-antisense 1; long non-coding; lung adenocarcinoma; prognosis, apoptosis.

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Conflict of interest statement

Competing Interests: The authors have declared that no competing interest exists.

Figures

Figure 1
Figure 1
Flow chart of data analysis. TCGA: the cancer genome atlas, GTEx: the genotype-tissue expression, LncRNA: long non-coding RNA, VIM-AS1: vimentin antisense RNA1, qPCR: quantitative rea-time PCR, COX: cox proportional-hazards model.
Figure 2
Figure 2
Expression feature of VIM-AS1 in lung cancer. (A-B) Expression of VIM-AS1 based on TCGA and GTEx dataset. (C) Expression levels of VIM-AS1 in paired adjacent normal tissues and paired samples. ***P<0.001.
Figure 3
Figure 3
Expression levels of VIM-AS1 were assessed using qPCR. **P<0.01.
Figure 4
Figure 4
Kaplan-Meier survival curves showed that low VIM-AS1 expression levels in LUAD patients are associated with poor overall survival OS (A), disease-specific survival DSS (B), and progression-free survival (PFI) (C).
Figure 5
Figure 5
Correlation between VIM-AS1 expression and clinical parameters includes pathological and TNM stages. (A-B) T-stage; (C) lymph node metastasis; (D-F) pathological stage; (G) gender; (H) residual tumor; (I) OS; (J) DSS; (K) PFI. *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001.
Figure 6
Figure 6
Construction and performance validation of the VIM-AS1-based nomogram for (A) OS; (B) DSS; (C) PFI in LUAD patients.
Figure 7
Figure 7
Biological functions of VIM-AS1 co-expressed genes.
Figure 8
Figure 8
VIM-AS1 overexpression influences A549 cell apoptosis. (A-C) Up-regulating lncVIM-AS1 increases the apoptosis rate in A549 detected by FCM. (D) Apoptosis-related proteins are tested by Western blot. * P<0.05, ***P<0.001.
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