Abstract
The effectiveness of selective drug therapy for cancer patients has gained much attention from academics and society. However, the rapid development of the drug resistance gained is becoming a significant challenge. As an essential catabolic and homeostatic process, autophagy plays a vigorous role in the degradation or recycling of proteins and cellular components, by which eukaryotic cells recycle or degrade their internal constituents through the machinery of membrane trafficking. Therefore, under traumatic conditions autophagy provides the cells with a safe supply of biomolecules and energy to maintain homeostasis. Deregulation of autophagy pays to tumor genesis, tumor-stromal interactions, and resistance to cancer therapies. Outcome of these interactions between plants and viruses, autophagy performs a vital role in regulating immune-related cell death, antiviral defense, and viral pathogenesis. This study explores the role of autophagy in drug resistance by identifying the mechanism by which autophagy is elaborate in drug resistance, focusing on its mode of action and validation as a potential therapy. Keywords: Autophagy mechanism; Cancer; ULK1/2 inhibitors
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