NRBP1 negatively regulates SALL4 to reduce the invasion and migration, promote apoptosis and increase the sensitivity to chemotherapy drugs of breast cancer cells.

Abstract

The incidence of breast cancer (BC) ranks first among all kinds of female malignancies. Its invasion, migration, apoptosis and resistance to chemotherapeutic drugs are the focus of current research. Nuclear receptor binding protein 1 (NRBP1) and spalt-like transcription factor 4 (SALL4), which are observed to be abnormally expressed in BC, are investigated herein to identify their involvement in invasion, migration, apoptosis and chemotherapeutic drug sensitivity of BC and to elucidate the underlying mechanism. After NRBP1 was overexpressed by cell transfection, wound healing and Transwell experiments were used to detect the abilities of cell invasion and migration, and western blotting was used to detect the expression of MMP2 and MMP9. Cell viability and apoptosis were detected by Cell Counting Kit-8 assay, TUNEL staining and western blotting, in which Doxorubicin (DOX) and cis-platinum (Cis) were administrated after overexpression of NRBP1. Finally, after overexpression of NRBP1 and SALL4, the cell invasion, migration and apoptosis, and the sensitivity to DOX and Cis, were detected to explore the underlying mechanism. Overexpression of NRBP1 inhibited the invasion and migration, promoted the apoptosis, and enhanced the chemotherapeutic effect of chemotherapy drugs in BC cells. Overexpression of SALL4 in cells blocked the effects of NRBP1 overexpression on invasion, migration, apoptosis and DOX and Cis drug sensitivity of BC cells. In conclusion, NRBP1 negatively regulated SALL4 to reduce the invasion and migration capacities, promote apoptosis and increase the sensitivity to chemotherapeutic drugs of BC cells.