The apatinib inhibits breast cancer cell line MDA-MB-231 in vitro by inducing apoptosis, cell cycle arrest, and regulating nuclear factor-κB (NF-κB) and mitogen-activated protein kinase (MAPK) signaling pathways.

Abstract

Breast cancer is one of the most common cancers and leading causes of death in the women worldwide. The evidence shows efficacy of apatinib against breast cancer. Accordingly, the present study was conducted to investigate the effect of apatinib on apoptosis, cell cycle, and Mitogen‑Activated Protein Kinase (MAPK) and nuclear factor-κB (NF-κB) signaling pathways in the breast cancer MDA-MB-231 cell line. The effects of apatinib on viability, morphology, tumor spheroid, cell cycle, migration, invasion, and apoptosis of MDA-MB-231 breast cancer cells were evaluated in vitro. In addition, expression of proteins involved in NF-κB and MAPK signaling pathways was evaluated using the western blotting analysis. Apatinib decreased viability, tumor spheroid, migration, and invasion of MDA-MB-231 cells. Furthermore, apatinib altered morphology and regulated cell cycle which followed by apoptosis induction in MDA-MB-231 cells. Apatinib decreased expression of p-p65 and p65 proteins in NF-κB signaling pathways and increased expression of p38, p-p38, JNK, and p-JNK in MAPK signaling pathways. The results suggested that apatinib can inhibit proliferation, migration and invasion of breast cancer cell line MDA-MB-231 through inducing apoptosis, cell cycle arrest, and regulating NF-κB and MAPK signaling pathways.