Unknown,Transcriptomics,Genomics,Proteomics

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Breast Cancer Progression in the Presence of Treated and Untreated Left Ventricular Dysfunction

ABSTRACT: We hypothesized that treating heart failure mitigates its impact on cancer progression and that different treatments (carvedilol, enalapril, empagliflozin) may have distinct effects. For this reason we have created an mouse model combining both heart failure (LAD ligation) and 4T1 metastatic breast cancer to study the effects of these treatments on breast cancer development at different levels: primary tumor growth in vivo, metastasis development and RNA-sequencing of the primary tumor. Twenty samples divided in five different groups were analyzed with RNA sequencing: group 1= Ctrl; group 2= HF/veh; group 3= HF/car; group 4= HF/emp group 5 HF/ena. HF medications with different mechanisms of action had distinct effects on 4T1 progression when the two diseases coexisted. These effects varied from isolated effects on the tumor transcriptome, to effects on the expansion of the primary tumor and on metastatic spread in the lungs.

INSTRUMENT(S): Illumina NovaSeq 6000

ORGANISM(S): Mus musculus

SUBMITTER: CELINE CIVATI

PROVIDER: E-MTAB-15506 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:We studied the effect of dietary fat type, varying in polyunsaturated/saturated fatty acid ratio's (P/S) on development of metabolic syndrome. C57Bl/6J mice were fed purified high-fat diets (45E% fat) containing palm oil (HF-PO; P/S 0.4), olive oil (HF-OO; P/S 1.1) or safflower oil (HF-SO; P/S 7.8) for 8 weeks. A low-fat palm oil diet (LF-PO; 10E% fat) was used as a reference. Additionally, we analyzed diet-induced changes in gut microbiota composition and mucosal gene expression. The HF-PO diet induced a higher body weight gain and liver triglyceride content compared to the HF-OO, HF-SO or LF-PO diet. In the intestine, the HF-PO diet reduced microbial diversity and increased the Firmicutes/Bacteroidetes ratio. Although this fits a typical obesity profile, our data clearly indicate that an overflow of the HF-PO diet to the distal intestine, rather than obesity itself, is the main trigger for these gut microbiota changes. A HF-PO diet-induced elevation of lipid metabolism-related genes in the distal small intestine confirmed the overflow of palm oil to the distal intestine. Some of these lipid metabolism-related genes were previously already associated with the metabolic syndrome. In conclusion, our data indicate that saturated fat (HF-PO) has a more stimulatory effect on weight gain and hepatic lipid accumulation than unsaturated fat (HF-OO and HF-SO). The overflow of fat to the distal intestine on the HF-PO diet induced changes in gut microbiota composition and mucosal gene expression. We speculate that both are directly or indirectly contributive to the saturated fat-induced development of obesity and hepatic steatosis. Keywords: Diet intervention study Nine-week-old C57Bl/6J mice were fed a low-fat diet (LF-PO) and three different types of high-fat diet, based on palm oil (HF-PO; P/S1.0), olive oil (HF-OO; P/S4.6) and safflower oil (HF-SO; P/S10.1) for 8 weeks. Body weight was recorded weekly and after 7 weeks of diet intervention an oral glucose tolerance test was performed. After 2 weeks of diet intervention, 6 mice per high-fat diet group were anaesthetized with a mixture of isofluorane (1.5%), nitrous oxide (70%) and oxygen (30%) and the small intestines were excised. Adhering fat and pancreatic tissue were carefully removed. The small intestines were divided in three equal parts along the proximal to distal axis (SI 1, SI 2 and SI 3) and microarray analysis was performed on mucosal scrapings.

Dataset Information

Breast Cancer Progression in the Presence of Treated and Untreated Left Ventricular Dysfunction

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