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Triple-negative breast cancer (TNBC) is associated with poor clinical prognosis due to a lack of effective therapeutic options. The expression of B-cell lymphoma/leukemia 11A (BCL11A) has been indicated to correlate with TNBC carcinogenesis, though the precise mechanisms of BCL11A-induced tumorigenesis in TNBC remain unclear. Using data retrieved from The Cancer Genome Atlas (TCGA) database, the present study demonstrated that BCL11A expression was upregulated in TNBC, compared with other types of breast cancer. Furthermore, in a tissue microarray of 140 patients with breast cancer, an elevated BCL11A level was correlated with unfavorable overall survival (OS), and exogenous BCL11A-knockdown was subsequently verified to inhibit tumor growth and metastasis in TNBC. Notably, the same tissue microarray revealed that a favorable patient outcome was associated with high expression levels of BCL11A and androgen receptor (AR). Moreover, BCL11A-knockdown significantly inhibited the expression level of AR and further had an influence on proliferation, migration and invasion in TNBC cell lines. Collectively, the results of the current study indicate the function of BCL11A in TNBC progression, and provide new insights into the unique mechanism of BCL11A in AR regulation, emphasizing the significance of more research on BCL11A and AR regulation in TNBC molecular treatment.

BCL11A confers cell invasion and migration in androgen receptor‑positive triple‑negative breast cancer