Mild dyslipidemia accelerates tumorigenesis through expansion of Ly6C^hi monocytes and differentiation to pro-angiogenic myeloid cells.

ABSTRACT: 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^hi 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 HFH

SUBMITTER: Tran T 

PROVIDER: S-EPMC9475043 | biostudies-literature | 2022 Sep

REPOSITORIES: biostudies-literature