Squamocin Suppresses Tumor Growth through Triggering an Endoplasmic Reticulum Stress‐Associated Degradation of EZH2/MYC Axis (Adv. Sci. 15/2025)

Endoplasmic Reticulum Stress Response Squamocin disrupts mitochondrial respiratory Complex I function, reduces ATP production, and impairs HSP90α function. These actions provoke endoplasmic reticulum (ER) stress and activate the unfolded protein response within tumor cells. This, in turn triggers the UBA6-UBE2ZFBXW7 ubiquitin cascade, enhancing ER stress-associated ubiquitylation and degradation of EZH2 and MYC, ultimately resulting in tumor growth arrest. More details can be found in article number 2413120 by Yunshan Ning and co-workers.