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CAVIN2/SDPR Functioned as a Tumor Suppressor in Lung Adenocarcinoma from Systematic Analysis of Caveolae-Related
Keyun Zhu1, Baichuan Wang2,3, Yingxi Li4
1Department of Thoracic Surgery, Ningbo Medical Centre Lihuili Hospital, Ningbo University, Ningbo, Zhejiang, P. R. China, 315040.
Abstract:
Background: Caveolae-Related Genes include caveolins and cavins, which are the main component of the fossa and, play important roles in a variety of physiological and pathological processes. Although increasing evidence indicated that caveolins (CAVs) and cavins (CAVINs) are involved in carcinogenesis and progression, their clinical significance and biological function in lung cancer are still limited. Methods: We investigated the expression of CAVs and CAVINs at transcriptional levels using Oncomine and Gene Expression Profiling Interactive Analysis. The protein and mRNA expression levels of CAVs and CAVINs were determined by the human protein atlas website and our surgically resected samples, respectively. The clinical value of prognostic prediction based on the expression of CAVs and CAVINs was also assessed. cBioPortal, GeneMANIA and STRING were used to analyze the molecular characteristics of CAVs and CAVINs in lung adenocarcinoma (LUAD) comprehensively. Finally, we investigated the effect of CAVIN2/SDPR (serum deprivation protein response) on LUAD cells with biological experiments in vitro. Results: The expression of CAV1/2 and CAVIN1/2/3 were significantly downregulated in LUAD and lung squamous cell carcinoma (LUSC). The patients with high expression of CAV1, CAV2, CAV3, CAVIN1 and CAVIN2/SDPR were tightly correlated with a better prognosis in LUAD, while no statistical significances in LUSC. Further, our results found that CAVIN2/SDPR can be identified as a prognostic biomarker independent of other CAVINs in patients with LUAD. Mechanically, the overexpression of CAVIN2/SDPR inhibited cell proliferation and migration owing to the cell apoptosis induction and cell cycle arrest at S phase in LUAD cells. Conclusions: CAVIN2/SDPR functioned as a tumor suppressor, and was able to serve as prognostic biomarkers in precision medicine of LUAD. Mechanically, overexpression of CAVIN2/SDPR inhibited cell proliferation by inducing cell apoptosis and S phase arrest in LUAD cells.
Insights
Caveolin and cavin gene expression is reduced in lung cancer. CAVIN2/SDPR acts as a tumor suppressor, inhibiting lung adenocarcinoma cell growth and migration, serving as a promising prognostic biomarker.
Area of Science:
- Molecular Biology
- Oncology
- Genetics
Background:
- Caveolae-related genes, including caveolins (CAVs) and cavins (CAVINs), are crucial for cellular processes.
- Their specific roles in lung cancer pathogenesis and clinical significance remain underexplored.
Purpose of the Study:
- To investigate the expression and clinical significance of CAVs and CAVINs in lung cancer.
- To elucidate the biological function of CAVIN2/SDPR in lung adenocarcinoma (LUAD).
Main Methods:
- Analysis of CAV and CAVIN expression at transcriptional and protein levels using public databases (Oncomine, GEPIA, Human Protein Atlas) and patient samples.
- Prognostic value assessment and molecular interaction analysis (cBioPortal, GeneMANIA, STRING).
- In vitro experiments to determine the functional role of CAVIN2/SDPR in LUAD cells.
Main Results:
- CAV1/2 and CAVIN1/2/3 expression were significantly downregulated in LUAD and lung squamous cell carcinoma (LUSC).
- High expression of CAV1, CAV2, CAV3, CAVIN1, and CAVIN2/SDPR correlated with better prognosis in LUAD, but not LUSC.
- CAVIN2/SDPR demonstrated independent prognostic value in LUAD and inhibited cell proliferation and migration by inducing apoptosis and S-phase arrest in vitro.
Conclusions:
- CAVIN2/SDPR functions as a tumor suppressor in LUAD.
- CAVIN2/SDPR is a potential prognostic biomarker for precision medicine in LUAD.
- Overexpression of CAVIN2/SDPR inhibits LUAD cell proliferation via apoptosis induction and cell cycle arrest.
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