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Background To explore the role of caveolin-1 (Cav-1) in breast cancer (BC). Methods Cav-1 expression data were downloaded from the Tumor Immune Estimation Resource (TIMER) and Gene Expression Omnibus (GEO) databases. We compared the expression of Cav-1 in different tumor tissues and between BC tissues and normal tissues (NTs), as well as the differences between different clinical traits. Kaplan-Meier survival analysis and univariate and multivariate Cox regression analyses were used to determine whether Cav-1 serves as a prognostic factor. The correlations of Cav-1 expression with the immune microenvironment and infiltrating immune cells were also analyzed. Quantitative polymerase chain reaction (qPCR) was used to detect Cav-1 mRNA expression in the MCF-7, SKB-R3, MDB-MB-231, and SUM-159 cell lines. LV-Cav-1-RNAi was transfected into MCF-7 and MDB-MB-231 cells, and the MTT assay was used to detect cell proliferation. Subsequently, MDB-MB-231 cells carrying the Cav-1-RNAi gene were used to determine the effects of Cav-1 knockdown on tumor growth in vivo using a severe combined immunodeficiency (SCID) model. Results Cav-1 was enriched in most solid tumors, and its expression was lower in BC tissues than in NT. Cav-1 expression was shown to be related to patients’ clinical outcomes. Cav-1 was expressed in the MCF-7, SKB-R3, MDB-MB-231, and SUM-159 cell lines. The MTT assay revealed that the proliferative ability of MDB-MB-231 and MCF-7 cells was accelerated. The tumor volume of SCID mice administered with LV-Cav-1-RNAi cells was increased. Conclusions These results suggest that Cav-1 may serve as a suppressor in the development of BC. |
