Mild dyslipidemia accelerates tumorigenesis through expansion of Ly6C monocytes and differentiation to pro-angiogenic myeloid cells.
Fiche publication
Date publication
septembre 2022
Journal
Nature communications
Auteurs
Membres identifiés du Cancéropôle Est :
Dr BRABENCOVA Eva, Pr MERROUCHE Yacine, Pr LE NAOUR Richard, Dr POTTEAUX Stéphane
Tous les auteurs :
Tran T, Lavillegrand JR, Lereverend C, Esposito B, Cartier L, Montabord M, Tran-Rajau J, Diedisheim M, Gruel N, Ouguerram K, Paolini L, Lenoir O, Pinteaux E, Brabencova E, Tanchot C, Urquia P, Lehmann-Che J, Le Naour R, Merrouche Y, Stockmann C, Mallat Z, Tedgui A, Ait-Oufella H, Tartour E, Potteaux S
Lien Pubmed
Résumé
Cancer and cardiovascular disease (CVD) share common risk factors such as dyslipidemia, obesity and inflammation. However, the role of pro-atherogenic environment and its associated low-grade inflammation in tumor progression remains underexplored. Here we show that feeding C57BL/6J mice with a non-obesogenic high fat high cholesterol diet (HFHCD) for two weeks to induce mild dyslipidemia, increases the pool of circulating Ly6C monocytes available for initial melanoma development, in an IL-1β-dependent manner. Descendants of circulating myeloid cells, which accumulate in the tumor microenvironment of mice under HFHCD, heighten pro-angiogenic and immunosuppressive activities locally. Limiting myeloid cell accumulation or targeting VEGF-A production by myeloid cells decrease HFHCD-induced tumor growth acceleration. Reverting the HFHCD to a chow diet at the time of tumor implantation protects against tumor growth. Together, these data shed light on cross-disease communication between cardiovascular pathologies and cancer.
Mots clés
Animals, Carcinogenesis, pathology, Cell Transformation, Neoplastic, pathology, Dyslipidemias, pathology, Inflammation, pathology, Mice, Mice, Inbred C57BL, Monocytes, pathology, Myeloid Cells, pathology, Tumor Microenvironment
Référence
Nat Commun. 2022 09 14;13(1):5399