Targeting Autophagy Pathways in Cancer Therapy: Cellular Mechanisms and Therapeutic Strategies
Received Date: Jun 01, 2024 / Published Date: Jun 27, 2024
Abstract
Autophagy, a fundamental cellular process involved in maintaining homeostasis through the degradation and recycling of cellular components, plays a dual role in cancer biology, influencing both tumor progression and response to therapy. This review examines the intricate cellular mechanisms regulating autophagy in cancer cells and discusses its potential as a therapeutic target. Key signaling pathways governing autophagy, including mTOR, AMPK, and Beclin-1 complexes, are explored in the context of their dysregulation in cancer and implications for therapeutic intervention.
Strategies to modulate autophagy in cancer therapy are reviewed, encompassing pharmacological agents that induce or inhibit autophagy, alone or in combination with conventional treatments. These approaches aim to exploit autophagy as a means to enhance treatment efficacy, overcome therapy resistance, and mitigate metastatic potential. Challenges in targeting autophagy, such as off-target effects and adaptive resistance mechanisms, are discussed, along with emerging technologies and biomarkers to improve patient stratification and therapeutic outcomes.
Future directions include advancing our understanding of the interplay between autophagy and other cellular processes, such as apoptosis and immune responses, and leveraging this knowledge to develop personalized therapeutic strategies. Ultimately, harnessing autophagy modulation in cancer therapy holds promise for advancing precision medicine and improving clinical outcomes for cancer patients.
Citation: Christoffer T (2024) Targeting Autophagy Pathways in Cancer Therapy:Cellular Mechanisms and Therapeutic Strategies. J Cell Mol Pharmacol 8: 215.
Copyright: © 2024 Christoffer T. This is an open-access article distributed underthe terms of the Creative Commons Attribution License, which permits unrestricteduse, distribution, and reproduction in any medium, provided the original author andsource are credited.
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