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Genome-wide analysis of gene expression in Calu-1 cells treated with cholesterol synthesis inhibitors

ABSTRACT: The hypothesis tested in this experiment was that a statin caused a larger shift in genes associated with pluripotency when compared with a Δ-24 oxidoreductase. It was theorized that the effect of the statin would be greater since the enzyme inhibition takes place proximal to the pathway branch involved in signal isoprenylation, whereas the oxidoreductase inhibits distal to this branch.

ORGANISM(S): Homo sapiens

PROVIDER: GSE47458 | GEO | 2015/10/14

SECONDARY ACCESSION(S): PRJNA205697

REPOSITORIES: GEO

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Genome-wide analysis of gene expression in MDA-MB-231 cells treated with cholesterol synthesis inhibitors

Project description:The hypothesis tested in this experiment was that a statin caused a larger shift in genes associated with pluripotency when compared with a Δ-24 oxidoreductase. It was theorized that the effect of the statin would be greater since the enzyme inhibition takes place proximal to the pathway branch involved in signal isoprenylation, whereas the oxidoreductase inhibits distal to this branch.

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Project description:Background: Clinical data identified an association between the use of HMG-CoA reductase inhibitors (statins) and incident diabetes in patients with underlying diabetes risk factors such as obesity, hypertension and dyslipidemia. The molecular mechanisms however are unknown. Methods: An observational cross-sectional study included 910 severely obese patients, mean (SD) body mass index 46.7 (8.7), treated with or without statins (ABOS cohort: a biological atlas of severe obesity). Data and sample collection took place in France between 2006 and 2016. Transcriptomic signatures of statin treatment in human liver obtained from genome-wide transcriptomic profiling of five different statin drugs using microarrays were correlated to clinico-biological phenotypes and also assigned to biological pathways and mechanisms. Results: We determined the hepatic, statin-related gene signature from genome-wide transcriptomic profiling in severely obese patients with varying degrees of glucose tolerance and cardio-metabolic comorbidities. Patients on statin treatment showed higher diabetes prevalence (OR=2.67; 95%CI, 1.60-4.45; P= 0.0002) and impairment of glucose homeostasis. This phenotype was associated with molecular signatures of increased hepatic de novo lipogenesis (DNL) via activation of sterol regulatory element-binding protein-1 (SREBP1) and concomitant upregulation of the expression of key genes in both fatty acid and triglyceride metabolism. Conclusions: DNL gene activation profile in response to statins was associated with insulin resistance and the diabetic status of the patients. Identified molecular signatures thus suggest that statin treatment increases the risk for diabetes in humans at least in part via induction of DNL.

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