A potential estrogen receptor inhibitor compound 34 induces apoptosis via ROS-independent intrinsic apoptosis in MCF-7 cells

Abstract

This study aimed to investigate the anti-tumor effect of the compound 34 on MCF-7 cells in vitro and explore its mechanisms. The MTT assay results showed that the compound 34 selectively inhibited the estrogen receptor-positive cells proliferation. Hoechst 33342 staining showed nuclear pyknosis, nuclear debris associated with apoptotic bodies. JC-1 staining showed the loss of mitochondrial membrane potential. Although the compound increased the intracellular reactive oxygen species (ROS), the apoptosis was not prevented by pretreatment with ROS scavengers. The Western blotting showed apoptosis-related protein like cytochrome c, and cleaved PARP protein increased. Furthermore, docking studies exhibited that the compound could bind to ERα. In summary, compound 34 selectively inhibited the estrogen receptor positive cells proliferation and induced apoptosis in MCF-7 cells via ROS-independent intrinsic apoptosis in MCF-7 cells. It may be a potential targeted drug of estrogen receptor for therapeutic application of breast cancer.

Keywords

• Apoptosis
• Compound 34
• Estrogen receptor
• MCF-7 cell