TY - CHAP
T1 - The Multifaceted Effects of Autophagy on the Tumor Microenvironment
AU - Kang, Rui
AU - Zeh, Herbert
AU - Lotze, Michael
AU - Tang, Daolin
N1 - Publisher Copyright:
© 2020, Springer Nature Switzerland AG.
PY - 2020
Y1 - 2020
N2 - The tumor microenvironment is composed of cancer cells, noncancer cells (e.g., immune cells, stromal cells, endothelial cells, and adipocytes), and various mediators (e.g., cytokines, chemokines, growth factors, and humoral factors) that work together to support cancer growth, progression, and resistance to therapies. Autophagy is an evolutionarily conserved degradation mechanism by which various cytosolic cargos (e.g., damaged organelles, unused molecules, or invaded pathogens) are engulfed by double-membrane autophagosomes, and then delivered into the lysosome for degradation and recycling. The level of autophagy is a crucial threshold to either promote cell survival or induce cell death in response to environmental stresses. Autophagy plays a context-dependent role in tumorigenesis and anticancer therapy via shaping the inflammatory, hypoxic, immunosuppressive, and metabolic tumor microenvironment. In particular, impaired autophagy flux is associated with chronic inflammation, immunosuppression, stromal formation, cancer stemness, angiogenesis, metastasis, and metabolic reprogramming in the tumor microenvironment. Understanding the molecular machinery of autophagy and its communication with hallmarks of cancer could lead to potential new anticancer strategies or drugs.
AB - The tumor microenvironment is composed of cancer cells, noncancer cells (e.g., immune cells, stromal cells, endothelial cells, and adipocytes), and various mediators (e.g., cytokines, chemokines, growth factors, and humoral factors) that work together to support cancer growth, progression, and resistance to therapies. Autophagy is an evolutionarily conserved degradation mechanism by which various cytosolic cargos (e.g., damaged organelles, unused molecules, or invaded pathogens) are engulfed by double-membrane autophagosomes, and then delivered into the lysosome for degradation and recycling. The level of autophagy is a crucial threshold to either promote cell survival or induce cell death in response to environmental stresses. Autophagy plays a context-dependent role in tumorigenesis and anticancer therapy via shaping the inflammatory, hypoxic, immunosuppressive, and metabolic tumor microenvironment. In particular, impaired autophagy flux is associated with chronic inflammation, immunosuppression, stromal formation, cancer stemness, angiogenesis, metastasis, and metabolic reprogramming in the tumor microenvironment. Understanding the molecular machinery of autophagy and its communication with hallmarks of cancer could lead to potential new anticancer strategies or drugs.
KW - Angiogenesis
KW - Autophagy
KW - Cancer stem cells
KW - Cell death
KW - Cytokine
KW - Ferroptosis
KW - Fibroblast
KW - Fibroblast
KW - Hypoxia
KW - Immune cells
KW - Immunosuppression
KW - Inflammation
KW - Metabolic reprogramming
KW - Metastasis
KW - Tumor microenvironment
UR - http://www.scopus.com/inward/record.url?scp=85079080409&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85079080409&partnerID=8YFLogxK
U2 - 10.1007/978-3-030-35727-6_7
DO - 10.1007/978-3-030-35727-6_7
M3 - Chapter
C2 - 32030650
AN - SCOPUS:85079080409
T3 - Advances in Experimental Medicine and Biology
SP - 99
EP - 114
BT - Advances in Experimental Medicine and Biology
PB - Springer
ER -