Abstract
Autophagy is a conserved cellular process required to maintain homeostasis. The hallmark of autophagy is the formation of a phagophore that engulfs cytosolic materials for degradation and recycling to synthesize essential components. Basal autophagy is constitutively active under normal conditions and it could be further induced by physiological stimuli such as hypoxia, nutrient starvation, endoplasmic reticulum stress,energy depletion, hormonal stimulation and pharmacological treatment. In cancer, autophagy is highly context-specific depending on the cell type, tumour microenvironment, disease stage and external stimuli. Recently, the emerging role of autophagy as a double-edged sword in cancer has gained much attention. On one hand, autophagy suppresses malignant transformation by limiting the production of reactive oxygen species and DNA damage during tumour development. Subsequently, autophagy evolved to support the survival of cancer cells and promotes the tumourigenicity of cancer stem cells at established sites. Hence, autophagy is an attractive target for cancer therapeutics and researchers have been exploiting the use of autophagy modulators as adjuvant therapy. In this review, we present a summary of autophagy mechanism and controlling pathways, with emphasis on the dual-role of autophagy (double-edged sword) in cancer. This is followed by an overview of the autophagy modulation for cancer treatment and is concluded by a discussion on the current perspectives and future outlook of autophagy exploitation for precision medicine.
Highlights
Cells are naturally safeguarded by an efficient check-andbalance mechanism better known as cellular homeostasis to maintain the balance of a wide array of biochemical factors and processes
Activated unc-51-like kinase 1 (ULK1) complex serves as a scaffolding unit to recruit class III phosphatidylinositol 3-kinase (PI3KIII) complex that consist of vacuolar protein sorting 34 (VPS 34), Beclin-1, VPS15 and ATG14-like (ATG14L) [9, 10]
The autophagy-related genes involved in the sequential process of autophagy mechanism, from initiation to degradation γ-aminobutyric-acid type A receptor-associated proteins (GABARAPs) and Golgi-associated ATPase enhancer of 16 kDa (GATE-16) subfamilies based on their amino acid sequence homology [15]
Summary
Cells are naturally safeguarded by an efficient check-andbalance mechanism better known as cellular homeostasis to maintain the balance of a wide array of biochemical factors and processes. The role of autophagy is rather controversial as it prevents malignant transformation and promotes tumour growth. Autophagy as tumour promoter As the tumour develops and progresses, autophagy, in turn, fuels and supports the growth of cancer cells.
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