Abstract
Triple-negative breast cancer (TNBC) refers to breast cancer without significant expression of estrogen receptor (ER), progesterone receptor (PR), or human epidermal growth factor receptor 2. We sought to identify the hub genes and find the potential progression mechanism of TNBC as well as immunotherapeutic targets. First, we screened the overlapped hub genes of Immune and Stromal, and the tumor mutation burden gene sets, as well as the The Cancer Genome Atlas (TCGA)-TNBC data set. Among these hub genes, we performed gene set enrichment analysis (GSEA) and gene set variation analysis analyses to recognize and evaluate the hub genes. Moreover, immune cell infiltration was evaluated by the CIBERSORT algorithm and single-sample GSEA. In addition, the expression and methylation of scavenger receptor class A member 5 (SCARA5) in TNBC were verified by quantitative PCR and methylation-specific PCR. Also, MTT and transwell assays were used to assess the biological function of SCARA5 in TNBC. SCARA5 and CMA1 were listed, and they mainly participated in cancer-related signaling pathways and immune-related signaling pathways. Interestingly, SCARA5 was closely associated with tumor purity and immune cell infiltration. Moreover, we found that SCARA5 was significantly downregulated and hypermethylation was in the promoter of SCARA5 in TNBC tissues. Our study showed the role of SCARA5 in proliferation and migration of TNBC, and suggested that SCARA5 can potentially serve as a candidate immunotherapy target for TNBC.
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