Tunicamycin-Induced Endoplasmic Reticulum Stress Promotes Breast Cancer Cell MDA-MB-231 Apoptosis through Inhibiting Wnt/β-Catenin Signaling Pathway

Figure 4

Mechanism of tunicamycin-induced ER stress promotes breast cancer cell MDA-MB-231 apoptosis. Tunicamycin is an activator of ER stress. It inhibits the ER glycosylation process and causes ER stress. After ER stress is activated, it inhibits the Wnt signaling pathway. When this pathway is suppressed, β-catenin phosphorylation is increased, resulting in a decrease in nuclear β-catenin, affecting the activation of downstream gene c-Myc transcription, and ultimately promoting breast cancer cell MDA-MB-231 apoptosis.