| Literature DB >> 33107196 |
Caner Yelek1,2, Lionel Mignion1, Nicolas Joudiou3, Romano Terrasi4, Florian Gourgue1,2, Matthias Van Hul2, Nathalie Delzenne2, Bernard Gallez1, Cyril Corbet5, Giulio G Muccioli4, Olivier Feron5, Patrice D Cani2, Bénédicte F Jordan1.
Abstract
Acetate is reported as a regulator of fat mass but also as lipogenic source for cancer cells. Breast cancer is surrounded by adipose tissue and has been associated with obesity. However, whether acetate contributes to cancer cell metabolism as lipogenic substrate and/or by changing fat storage and eventually obesity-induced breast cancer progression remains unknown. Therefore, we studied the contribution of acetate to breast cancer metabolism and progression. In vitro, we found that acetate is not a bioenergetic substrate under normoxia and did not result in a significant change of growth. However, by using lipidomic approaches, we discovered that acetate changes the lipid profiles of the cells under hypoxia. Moreover, while mice fed a high-fat diet (HFD) developed bigger tumours than their lean counterparts, exogenous acetate supplementation leads to a complete abolishment of fat mass gain without reverting the HFD-induced obesity-driven tumour progression. In conclusion, although acetate protects against diet-induced obesity, our data suggest that it is not affecting HFD-driven tumour progression.Entities:
Keywords: acetate; high-fat diet; hypoxia; metabolism; obesity; tumour growth
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Year: 2020 PMID: 33107196 PMCID: PMC7753876 DOI: 10.1111/jcmm.16034
Source DB: PubMed Journal: J Cell Mol Med ISSN: 1582-1838 Impact factor: 5.295