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Autophagy is a catabolic mechanism crucial for sustaining cellular homeostasis, and in this process, encapsulated degraded inside repurposed to facilitate metabolic processes. In cancer, autophagy has a dual role: it acts as a tumor suppressor by preventing the buildup of damaged cellular components, but also as a survival mechanism, that supports tumor growth under stress. Cancer cells often trigger autophagy to manage the increased metabolic demands of rapid growth. This stress tolerance allows tumor cells to maintain energy production, contributing to both tumor progression and resistance to treatment. Preclinical studies have shown that autophagy inhibition reinstates chemotherapeutic sensitivity and increases tumor cell mortality. These findings indicate that targeting autophagy may represent a viable therapeutic approach, with early-phase clinical trials exploring the use of hydroxychloroquine alongside chemotherapy or targeted treatments. As comprehension of autophagy in oncology advances, there is an increasing interest in creating more targeted and efficacious autophagy inhibitors for therapeutic applications.
Jha et al. (Tue,) studied this question.
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