The endoplasmic reticulum is a vital intracellular organelle that plays a pivotal role in various cellular processes, including lipid synthesis, the folding and secretion of transmembrane proteins, and the maintenance of intracellular homeostasis. When cells are affected by internal or external stimuli that disrupt the homeostasis of the internal environment, the endoplasmic reticulum signalling sensors respond to the internal disorder by stressing the endoplasmic reticulum and activating the unfolded protein response downstream as a cellular activation and protection mechanism to restore the qualitative and quantitative balance of intracellular proteins. Sustained or high-intensity endoplasmic reticulum stress activates cellular autophagy, which mitigates oxidative damage by degrading damaged organelles or excess cytoplasm and maintains normal cellular physiological activities.ER homeostasis and autophagy are essential for a variety of tumor development, metastasis, and chemoresistance. And ERS emits multiple signals to induce autophagy, which exerts cytoprotective effects. Therefore, targeting ERS and its mediated autophagy may be a viable approach for the development of new cancer therapies. In this review, we review the interrelationship between endoplasmic reticulum stress and autophagy based on the latest research advances, and explore the mechanism of action of the two in tumor drug resistance to develop potential positive clinical outcomes. |