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BACH1 is overexpressed in prostate cancer. Because this promotes invasion and migration, it may facilitate metastasis of prostate cancer. Thus, BACH1 is a potential therapeutic target for metastatic prostate cancer. BACH1 silencing therapy can be considered as a novel and effective adjuvant in prostate cancer targeted therapies.

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During breast cancer progression, tumor cells acquire multiple malignant features. The transcription factors and cell cycle regulators high mobility group A2 (HMGA2) and BTB and CNC homology 1 (Bach‐1) are overexpressed in several cancers, but the mechanistic understanding of how HMGA2 and Bach‐1 promote cancer development has been limited. We found that HMGA2 and Bach‐1 are overexpressed in breast cancer tissues and their expression correlates positively in tumors but not in normal tissues. Individual HMGA2 or Bach‐1 knockdown downregulates expression of both proteins, suggesting a mutual stabilizing effect between the two proteins. Importantly, combined HMGA2 and Bach‐1 knockdown additively decrease cell proliferation, migration, epithelial‐to‐mesenchymal transition, and colony formation, while promoting apoptotic cell death via upregulation of caspase‐3 and caspase‐9. First the first time, we show that HMGA2 and Bach‐1 overexpression in tumors correlate positively and that the proteins cooperatively suppress a broad range of malignant cellular properties, such as proliferation, migration, clonogenicity, and evasion of apoptotic cell death. Thus, our observations suggest that combined targeting of HMGA2 and Bach1 may be an effective therapeutic strategy to treat breast cancer.