Autophagy Paradox of Cancer: Role, Regulation, and Duality

Amit Kumar Verma, Prahalad Singh Bharti, Sahar Rafat, Deepti Bhatt, Yamini Goyal, Kamlesh Kumar Pandey, Sanjeev Ranjan, Saleh A. Almatroodi, Mohammed A. Alsahli, Arshad Husain Rahmani, Ahmad Almatroudi, Kapil Dev*

*Corresponding author for this work

Research output: Contribution to journalReview Articlepeer-review

43 Citations (Scopus)

Abstract

Autophagy, a catabolic process, degrades damaged and defective cellular materials through lysosomes, thus working as a recycling mechanism of the cell. It is an evolutionarily conserved and highly regulated process that plays an important role in maintaining cellular homeostasis. Autophagy is constitutively active at the basal level; however, it gets enhanced to meet cellular needs in various stress conditions. The process involves various autophagy-related genes that ultimately lead to the degradation of targeted cytosolic substrates. Many factors modulate both upstream and downstream autophagy pathways like nutritional status, energy level, growth factors, hypoxic conditions, and localization of p53. Any problem in executing autophagy can lead to various pathological conditions including neurodegeneration, aging, and cancer. In cancer, autophagy plays a contradictory role; it inhibits the formation of tumors, whereas, during advanced stages, autophagy promotes tumor progression. Besides, autophagy protects the tumor from various therapies by providing recycled nutrition and energy to the tumor cells. Autophagy is stimulated by tumor suppressor proteins, whereas it gets inhibited by oncogenes. Due to its dynamic and dual role in the pathogenesis of cancer, autophagy provides promising opportunities in developing novel and effective cancer therapies along with managing chemoresistant cancers. In this article, we summarize different strategies that can modulate autophagy in cancer to overcome the major obstacle, i.e., resistance developed in cancer to anticancer therapies.

Original languageEnglish
Article number8832541
JournalOxidative Medicine and Cellular Longevity
Volume2021
DOIs
Publication statusPublished - 2021
MoE publication typeA2 Review article, Literature review, Systematic review

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