Unraveling the Mechanisms of AhR-Notch Interplay in Mediating Arsenic Trioxide Cytotoxicity in MCF-7 and MDA-MB-231 Breast Cancer Cell Lines.

Arsenic trioxide (ATO) induces oxidative stress and apoptotic cell death in cancer cells; however, the underlying mechanisms and its effects on other signaling pathways, particularly in breast cancer, remain inadequately understood. The aryl hydrocarbon receptor (AhR) is expressed in breast cancer cells and linked to disease progression, while Notch signaling enhances migratory properties in these cells. The simultaneous use of the AhR agonist (FICZ), AhR antagonist (CH223191), and Notch antagonist (DAPT) was intended to investigate how the modulation of these pathways affects the response of breast cancer cells (MDA-MB-231 and MCF-7 cell) to ATO.