Modulating Autophagy as an Attractive Strategy to Treat Renal Cell Carcinoma

Autophagy is a key major mechanism by which cancer cells are able to survive periods of therapy-induced stress that result in drug resistance, autophagy is crucial for mediating cellular stress and damage. Renal Cell Carcinomas (RCC) make up about 90% of kidney cancer cases. Modulating autophagy has been demonstrated to increase the cytotoxicity of authorized Renal Cell Carcinoma (RCC) therapies and combat drug resistance in recent years. Autophagy activation inhibits malignancies by removing damaged organelles and proteins while shielding certain tumor cells from low oxygen levels and starvation, which are primary features of tumor microenvironments. It is unknown why autophagy has two effects, despite evidence that it controls both cell death and survival. Research has shown that autophagy regulators can treat RCC by controlling the PI3K/Akt/mTOR and AMPK/mTOR signaling pathways. On the other hand, the relationship between autophagy and immune cell activation, especially in RCC, is unclear. Early studies suggest inhibiting autophagy can affect hematopoiesis and systemic immunity, suggesting immune checkpoint inhibitor therapy may not be beneficial. Recent studies show autophagy inhibition does not stop T-cell activation. It is noteworthy that studies examining the connection between autophagy and RCC are becoming more popular. Autophagy-related proteins have been shown in earlier research to be interesting prognostic indicators for Renal Cell Carcinoma (RCC) treatment. Therefore, to determine the therapeutic relevance of autophagy activators and inhibitors in Renal cell carcinomas (RCC), more investigation is required. This study explores the therapeutic alternatives for the current situation and potential future directions of autophagy targeting as a potential alternative and successful treatment for renal cell carcinoma.