Exploring the Emerging Role of Autophagy in Governing Cellular Dormancy

Bhavya Fenoy^*
*Correspondence: Bhavya Fenoy, Department of Neuro-Oncology, Russian People’s Friendship University, 121359 Moscow, Russia, Email:

Introduction

Cellular dormancy, a state of reversible growth arrest, is a fundamental survival strategy adopted by cells in response to various intrinsic and extrinsic cues, including nutrient deprivation, hypoxia and exposure to environmental stressors. Dormant cells exhibit reduced metabolic activity, suppressed proliferation and enhanced resistance to cytotoxic insults, enabling them to evade immune surveillance and withstand adverse conditions. While the concept of cellular dormancy has long been recognized in the context of cancer metastasis and microbial persistence, recent advances in molecular biology have unveiled the intricate role of autophagy, a conserved cellular degradation process, in governing the induction, maintenance and exit from dormancy. This essay elucidates the emerging role of autophagy in regulating cellular dormancy, delineating the underlying mechanisms, physiological implications and therapeutic implications [1].

Autophagy is a fundamental cellular process involved in the degradation and recycling of cellular components. It plays a crucial role in maintaining cellular homeostasis by eliminating damaged organelles, protein aggregates and intracellular pathogens. The process of autophagy involves the formation of double-membraned vesicles called autophagosomes, which engulf cytoplasmic cargo targeted for degradation. These autophagosomes then fuse with lysosomes, forming autolysosomes, where the cargo is degraded by lysosomal hydrolases. Autophagy is tightly regulated by a complex network of signaling pathways, including the mammalian Target of Rapamycin (mTOR) pathway, AMP-Activated Protein Kinase (AMPK) pathway and various Autophagy-related (ATG) proteins [2].

Description

Autophagy, a highly conserved catabolic process, plays a central role in maintaining cellular homeostasis by facilitating the degradation and recycling of damaged organelles, protein aggregates and intracellular pathogens. The canonical autophagy pathway involves the formation of double-membrane vesicles known as autophagosomes, which sequester cytoplasmic cargo and deliver it to lysosomes for degradation. Emerging evidence suggests that autophagy exerts a profound influence on the induction and maintenance of cellular dormancy through its ability to modulate key signaling pathways implicated in cell cycle regulation, metabolism and stress response. In conditions of nutrient deprivation or metabolic stress, autophagy serves as a crucial adaptive mechanism that enables cells to survive prolonged periods of quiescence. By degrading and recycling cellular components, autophagy replenishes intracellular nutrient pools, sustains energy production and preserves cellular viability during dormancy. Moreover, autophagy-mediated removal of damaged organelles and protein aggregates prevents the accumulation of toxic by-products, thereby safeguarding cellular integrity and function. Consequently, dysregulation of autophagy has been implicated in the pathogenesis of various diseases characterized by aberrant cellular dormancy, including cancer, neurodegenerative disorders and infectious diseases [3,4].

In the context of cancer biology, autophagy plays a dual role in regulating tumor dormancy and progression. While autophagy-mediated quiescence can confer resistance to chemotherapy and promote tumor recurrence, it may also serve as a tumor-suppressive mechanism by inhibiting cellular proliferation and metastatic dissemination. The balance between pro-survival and pro-apoptotic functions of autophagy in cancer dormancy remains a subject of ongoing investigation, with implications for the development of targeted therapies aimed at exploiting autophagy as a therapeutic vulnerability in dormant cancer cells. Furthermore, emerging evidence suggests that autophagy-mediated dormancy may play a critical role in microbial persistence and antibiotic tolerance. Bacterial pathogens, such as Mycobacterium tuberculosis and Salmonella enterica, can enter a dormant state within host cells, where they evade immune clearance and withstand antibiotic treatment. Autophagy represents a host defense mechanism that targets intracellular pathogens for lysosomal degradation, thereby restricting their replication and dissemination. However, certain pathogens have evolved strategies to subvert autophagy and exploit the host cell's autophagic machinery to promote their survival and persistence. Understanding the interplay between autophagy and microbial dormancy is essential for developing novel therapeutic approaches to combat persistent infections and antibiotic resistance [5].

Conclsuion

In conclusion, autophagy emerges as a central player in governing cellular dormancy, orchestrating the delicate balance between quiescence, survival and reactivation in response to diverse physiological and pathological stimuli. By regulating metabolic homeostasis, cellular integrity and stress adaptation, autophagy enables cells to cope with adverse environmental conditions and evade immune surveillance. Dysregulation of autophagy-mediated dormancy underlies the pathogenesis of various diseases, including cancer, neurodegenerative disorders and infectious diseases, highlighting its therapeutic potential as a target for intervention. Continued research efforts aimed at elucidating the molecular mechanisms governing the interplay between autophagy and cellular dormancy hold promise for uncovering novel therapeutic strategies to manipulate dormancy-associated pathways for clinical benefit. Through interdisciplinary collaboration and innovative approaches, the emerging role of autophagy in governing cellular dormancy offers new insights into fundamental cellular processes and opportunities for the development of precision medicine approaches to disease management.

Acknowledgement

None.

Conflict of Interest

None.

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