Breast cancer is the number one cause of death from malignant
tumors in women. The expression level of RAD51 in malignant
tumors is significantly higher than normal tissues and is closely related to
tumor progression, immunosuppression, resistance to
radiotherapy and
chemotherapy, and prognosis. We assess the role of RAD51 in
breast cancer via bioinformatics analysis. The expression of RAD51 in
breast cancer and its relationship with clinicopathology were analyzed by TCGA, GEPIA2, TIMER database; univariable survival and multivariate Cox analysis were used to compare several clinical characteristics with survival. We also explored the correlation between RAD51 and
cancer immune infiltrates cell level using cibersort and TIMER database. In addition, we used STRING, GeneMANIA, and GSEA analysis to explore RAD51 upstream and downstream regulatory
proteins, RAD51 family (RAD51, RAD51B, RAD51C, RAD51D, XRCC2, XRCC3, and DMC1) gene interaction network map, and RAD51 enrichment analysis. Finally, RAD51 genetic variation, functional enrichment analysis of adjacent genes, and RAD51 immunohistochemical expression in
breast cancer tissues were observed by cBioPortal, HPA database. RAD51 expression in
breast cancer,
lung adenocarcinoma, lung
squamous cell carcinoma,
gastric cancer,
colon adenocarcinoma, and
endometrial cancer are higher than normal tissues. In
breast cancer patients, the expression of RAD51 was significantly different due to age, T stage, and
tumor stage. The overall survival of RAD51 low-expression patients were better than high-expression patients (P = 0.018). Compared with the RAD51 low expression group, the M0 and M1 of activated CD4+ T cells, Tfh cells, Treg cells, and macrophages significantly increased in the high expression group; the initial B cells, resting CD4+ T cells, resting NK cells, resting dendritic cells, activated dendritic cells, resting mast cells, neutrophils significantly decreased; and RAD51 expression was significantly positively correlated with infiltration of B cells, CD4+ T cells, CD8/CD4+ T cells, neutrophils, and dendritic cells. STRING analysis showed the interaction between RAD51 and MND1, RAD52, BRCA2, CHEK1, BLM, EXO1, BRCA1, BARD1, MUS81, ATM. Matrix
transcription factor pathway, cell cycle pathway, DNA replication pathway, and P53 signaling pathway were identified as the differentially enriched pathway in KEGG. RAD51 is a prognostic
biomarker and correlated with immune infiltrates in
breast cancer.