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Autophagy in Cancer Metastasis

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Autophagy in Stem Cell Maintenance and Differentiation

Part of the book series: Stem Cell Biology and Regenerative Medicine ((STEMCELL,volume 73))

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Abstract

During cancer development, tumour cells are exposed to various intrinsic and extrinsic stresses such as nutrient deficiency, lack of oxygen, DNA damage, and growth factor deprivation that regulate cell growth and homeostasis. In response to these stresses, tumour cells, unlike healthy cells, develop adaptive strategies to grow and migrate successfully. One of the key mechanisms that cancer cells utilize to circumvent cellular stresses is autophagy, which is a catabolic process that facilitates the degradation and recycling of damaged organelles, thereby reducing cellular stress and promoting cell survival. Emerging studies have shown a vital role of autophagy in cancer metastasis, which is the major cause of cancer-associated deaths. However, the role of autophagy in metastasis is multidimensional and involves both metastasis-promoting and suppressing roles dependent on the demands of tumour cells during the metastatic process. As novel compounds targeting autophagy emerge, it will be crucial to consider the stage of metastatic progression at which autophagy is being targeted to efficiently overcome metastasis.

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Abbreviations

APP:

Amyloid precursor protein

ARHI:

Aplasia Ras homolog member I

ATF:

Activating transcription factor

ATG:

Autophagy-related gene

CAF:

Cancer-associated fibroblasts

CDCP1:

CUB domain-containing protein-1

CSF-1:

Colony stimulating factor 1

CTC:

Circulating tumour cell

CXC:

CXC-chemokine ligand

DIAPH3:

Diaphanous homologue 3

EC:

Endothelial cell

ECM:

Extracellular matrix

EGF:

Epidermal growth factor

EMT:

Epithelial-mesenchymal transition

ER:

Endoplasmic reticulum

ERK:

Extracellular-regulated kinase

FAK:

Focal adhesion kinase

FAS:

FS-7-associated surface antigen

HGF:

Hepatocyte growth factor

IGF:

Insulin-like growth factor

LC3:

Microtubule-associated protein 1 light chain 3

MAPK:

Mitogen-activated protein kinase

MET:

Mesenchymal-epithelial transition

MHC:

Major histocompatibility complex

MICA/B:

MHC-I polypeptide-related sequence A/B

MLCK:

Myosin light chain kinase

MMP:

Matrix metalloproteinase

mTOR:

Mechanistic target of rapamycin

NF-κB:

Nuclear factor kappa B

NK:

Natural killer

NKG2D:

Natural killer group 2D

NRF2:

NF-E2-related factor 2

PAR:

Protease-activated receptor

PERK:

Protein kinase R-like ER kinase

PI3K:

Phosphoinositide 3 kinase

PTEN:

Phosphate and tensin homolog

ROCK:

RhoA-Rho-associated protein kinase

ROS:

Reactive oxygen species

TAM:

Tumour-associated macrophage

TGFβ:

Transforming growth factor β

TKI:

Tyrosine kinase inhibitor

TME:

Tumour microenvironment

TNF:

Tumour necrosis factor

uPA:

Urokinase-type plasminogen activator

VCAM:

Vascular cell adhesion molecule

VEGF:

Vascular endothelial growth factor

ZEB1:

Zinc finger E-box binding homeobox 1

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Acknowledgements

Work in the laboratory of NR is supported by funds from Centre for Cancer Biology, University of South Australia and Neurosurgical Research Foundation (NRF), Adelaide, Australia.

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Polara, R., van Rinsum, D., Robinson, N. (2023). Autophagy in Cancer Metastasis. In: Shravage, B.V., Turksen, K. (eds) Autophagy in Stem Cell Maintenance and Differentiation. Stem Cell Biology and Regenerative Medicine, vol 73. Springer, Cham. https://doi.org/10.1007/978-3-031-17362-2_11

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