title: Adipocyte is a non-trivial, dynamic partner of breast cancer cells.
abstract: While the participation of adipocytes is well known in tissue architecture, energy supply and endocrine processes, their implication during natural cancer history is just beginning to unfold. An extensive review of the literature concerning the impact of resident adipocytes on breast cancer development/progression was performed. This review provides in vitro and in vivo evidence that adipocytes located close to invasive cancer cells, referred to as cancer-associated adipocytes (CAAs), are essential for breast tumor development/progression. Their deleterious function is dependent, at least partly, on their crosstalk with invasive cancer cells. Indeed, this event leads to dramatic phenotypic and/or functional modifications of both cell types. Adipocytes exhibit delipidation and acquire a fibroblast-like shape. In parallel, cancer cell aggressiveness is exacerbated through increased migratory and invasive properties. Moreover, obesity is currently a sign of poor prognosis in human carcinomas. In this context, a high number of "obese" resident adipocytes might be predicted to be detrimental. Accordingly, there are some similarities between the molecular alterations observed in hypertrophied adipocytes and in CAAs. How adipocytes function to favor tumorigenesis at the molecular level remains largely unknown. Nevertheless, progress has been made recently and molecular clues are starting to emerge. Deciphering the cellular and molecular mechanisms behind the adipocyte-cancer cell heterotypic crosstalk is of great interest since it might provide new targets for improving diagnosis/prognosis and for the design of innovative therapeutic strategies. They might also improve our understanding of the relationship between obesity/metabolic disorders and cancer risk and/or poor patient outcome.
authors.affiliation: Institut de Génétique et de Biologie Moléculaire et Cellulaire, Functional Genomics and Cancer Department, Centre National de la Recherche Scientifique UMR 7104, INSERM U964, Université de Strasbourg, France.
authors.forename: Jinxiang
authors.initials: J
authors.lastname: Tan
authors.forename: Emilie
authors.initials: E
authors.lastname: Buache
authors.forename: Marie-Pierre
authors.initials: MP
authors.lastname: Chenard
authors.forename: Nassim
authors.initials: N
authors.lastname: Dali-Youcef
authors.forename: Marie-Christine
authors.initials: MC
authors.lastname: Rio
mesh_terms: D017667:Adipocytes / Q000378:metabolism / Q000473:pathology*; D050156:Adipogenesis; D001943:Breast Neoplasms / Q000209:etiology / Q000378:metabolism / Q000473:pathology*; D002450:Cell Communication; D048909:Diabetes Complications / Q000378:metabolism / Q000473:pathology; D005109:Extracellular Matrix / Q000378:metabolism / Q000473:pathology; D005260:Female; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism; D007333:Insulin Resistance; D009361:Neoplasm Invasiveness / Q000473:pathology; D009765:Obesity / Q000150:complications / Q000378:metabolism / Q000473:pathology
chemical_list: D018836:Inflammation Mediators