Transcriptomic analysis of total RNA from melanoma tumor, originating from control and hyperlipic diet

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 two-week feeding of wildtype C57BL/6J mice with a high fat high cholesterol atherogenic diet (HFHCD) increases the pool of circulating Ly6C hi monocytes available for initial melanoma development, under the control of IL-1. 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 tumor growth acceleration under HFHCD. Reverting the HFHCD to a chow diet at the time of tumor implantation slows down tumor growth. Together, these data shed light on cross-disease communication between cardiovascular pathologies and cancer. The aim of the analysis is to compare the transcriptomic profile of primary solid tumors isolated from mice fed with a chow diet (CD) or a high fat high choleterol diet (HFHCD). C57BL/6J mice were fed a CD or HFHCD for 2 weeks before subcutaneous injection of B16-F10 melanoma cells. 4 tumors per group were harvested from mice fed with CD or HFHCD at day 9 post injection of B16-F10 melanoma cells to perform trasncriptomic arrays. Tumors were minced and lysed into RLT buffer containing 1% β-mercaptoethanol. RNA was extracted using Qiagen RNeasy kit according to the manufacturer’s instructions. Analysis of gene was done by affymetrix microarrays at de GENOM’IC core facility (Cochin Institute). Microarray analysis help to understand the molecular pathways involved in aggravation of tumor growth under HFHCD.