Interaction between adipose tissue and cancer cells: role for cancer progression
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NON-THEMATIC REVIEW
Interaction between adipose tissue and cancer cells: role for cancer progression Jean-François Dumas 1 & Lucie Brisson 1 Received: 28 July 2020 / Accepted: 22 September 2020 # Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract Environment surrounding tumours are now recognized to play an important role in tumour development and progression. Among the cells found in the tumour environment, adipocytes from adipose tissue establish a vicious cycle with cancer cells to promote cancer survival, proliferation, metastasis and treatment resistance. This cycle is particularly of interest in the context of obesity, which has been found as a cancer risk factor. Cancers cells can reprogram adipocyte physiology leading to an “activated” phenotype characterized by delipidation and secretion of inflammatory adipokines. The adipocyte secretions then influence tumour growth and metastasis which has been mainly attributed to interleukin 6 (IL-6) or leptin but also to the release of fatty acids which are able to change cancer cell metabolism and signalling pathways. The aim of this review is to report recent advances in the understanding of the molecular mechanisms linking adipose tissue with cancer progression in order to propose new therapeutic strategies based on pharmacological or nutritional intervention. Keywords Adipocyte . Cancer . Adipokines . Metabolism . Fatty acid . Exosome
Abbreviations AMPK AMP-activated protein kinase ATP adenosine triphosphate COX-2 cyclooxygenase-2 CPT1 carnitine palmitoyltransferase I EMT epithelial to mesenchymal transition FABP fatty acid-binding protein FATP1 fatty acid transport protein 1 GDF 15 growth differentiation factor 15 HIF-1 hypoxia-inducible transcription factor IGFBP-2 insulin-like growth factor binding protein-2 IL-6 interleukin 6 JAK Janus kinase JNK c-Jun N-terminal kinase LD lipid droplets MCP-1 macrophage chemoattractant protein MMP matrix metalloproteinase NK natural killer PGE2 prostaglandin E2
* Lucie Brisson [email protected] 1
Inserm UMR1069, Nutrition, Growth and Cancer, University of Tours, 10 boulevard Tonnellé, 37032 Tours, France
PLOD2 PPAR ROS STAT TGFβ UCP VHL
procollagen-lysine, 2-oxoglutarate 5-dioxygenase 2 peroxisome proliferator-activated receptors reactive oxygen species signal transducer and activator of transcription transforming growth factor beta uncoupling protein von Hippel-Lindau
1 Introduction Tumours are complex tissues composed of cancer and noncancer cells in a hypoxic and nutrient-deprived microenvironment. In order to survive, tumour cells need to adapt to these harsh conditions. One main property of cancer cells is their capacity to reprogram metabolism and take advantage of substrates available in the surrounding microenvironment [1]. Several types of cooperation have been demonstrated between cancer and non-cancer cells of the tumour, such as macrophages or fibroblasts [2]. Recently, the interaction of tumours with the surrounding adipose tissue has gained interest. Indeed, tumours, local
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