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

Abstract

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.