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Ecotropic viral integration site‑1 (EVI‑1) is an important transcription factor involved in oncogenesis. Aberrant EVI‑1 expression has been reported to be a characteristic of multiple types of malignancies; however, very little is known about how EVI‑1 regulates breast cancer. Current knowledge of how target genes mediate the biological function of EVI‑1 remains limited. In the present study, overexpression of EVI‑1 promoted cell proliferation, migration, and invasion, and inhibited apoptosis in breast cancer. By contrast, silencing of EVI‑1 inhibited cell proliferation, migration and invasion, and enhanced apoptosis in breast cancer. In addition, the results also revealed that the aberrant expression of EVI‑1 regulates genes associated with the apoptotic pathway in breast cancer. Furthermore, EVI‑1 was also likely to target the promoter region of calreticulin (CRT) in vitro. It was concluded that EVI‑1 can affect epithelial mesenchymal transition‑associated genes by regulating the expression of CRT in breast cancer. The results revealed that EVI‑1 may be a potential effective therapeutic target in breast cancer.

EVI‑1 acts as an oncogene and positively regulates calreticulin in breast cancer