The dual role of chaperone-mediated autophagy in the response and resistance to cancer immunotherapy

Abstract

Cancer immunotherapy has become a revolutionary strategy in oncology, utilizing the host immune system to fight malignancies. Notwithstanding major progress, obstacles such as immune evasion by tumors and the development of resistance still remain. This manuscript examines the function of chaperone-mediated autophagy (CMA) in cancer biology, focusing on its effects on tumor immunotherapy response and resistance. CMA is a selective degradation mechanism for cytosolic proteins, which is crucial for sustaining cellular homeostasis and regulating immune responses. By degrading specific proteins, CMA can either facilitate tumor progression in stressful conditions, or promote tumor suppression by removing oncogenic factors. This double-edged sword highlights the complexity of CMA in cancer progression and its possible effect on treatment results. Here we clarify the molecular mechanisms by which CMA can regulate the immune response and its possible role as a therapeutic target for improving the effectiveness of cancer immunotherapy.