{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Baek AE"],"funding":["NIDDK NIH HHS","NCI NIH HHS"],"pagination":["864"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC5636879"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["8(1)"],"pubmed_abstract":["Obesity and elevated circulating cholesterol are risk factors for breast cancer recurrence, while the use of statins, cholesterol biosynthesis inhibitors widely used for treating hypercholesterolemia, is associated with improved disease-free survival. Here, we show that cholesterol mediates the metastatic effects of a high-fat diet via its oxysterol metabolite, 27-hydroxycholesterol. Ablation or inhibition of CYP27A1, the enzyme responsible for the rate-limiting step in 27-hydroxycholesterol biosynthesis, significantly reduces metastasis in relevant animal models of cancer. The robust effects of 27-hydroxycholesterol on metastasis requires myeloid immune cell function, and it was found that this oxysterol increases the number of polymorphonuclear-neutrophils and γδ-T cells at distal metast"],"journal":["Nature communications"],"pubmed_title":["The cholesterol metabolite 27 hydroxycholesterol facilitates breast cancer metastasis through its actions on immune cells."],"pmcid":["PMC5636879"],"funding_grant_id":["R01 DK095842","R01 DK048807","R00 CA172357","R01 DK062777"],"pubmed_authors":["Kwon S","Sullivan PM","McDowell HB","Thompson JW","Gunn MD","Nelson ER","McDonnell DP","He S","Pillai RV","Dubois LG","Yu YA","Chang CY","Kemper JK","Wardell SE","Baek AE"],"additional_accession":[]},"is_claimable":false,"name":"The cholesterol metabolite 27 hydroxycholesterol facilitates breast cancer metastasis through its actions on immune cells.","description":"Obesity and elevated circulating cholesterol are risk factors for breast cancer recurrence, while the use of statins, cholesterol biosynthesis inhibitors widely used for treating hypercholesterolemia, is associated with improved disease-free survival. Here, we show that cholesterol mediates the metastatic effects of a high-fat diet via its oxysterol metabolite, 27-hydroxycholesterol. Ablation or inhibition of CYP27A1, the enzyme responsible for the rate-limiting step in 27-hydroxycholesterol biosynthesis, significantly reduces metastasis in relevant animal models of cancer. The robust effects of 27-hydroxycholesterol on metastasis requires myeloid immune cell function, and it was found that this oxysterol increases the number of polymorphonuclear-neutrophils and γδ-T cells at distal metast","dates":{"release":"2017-01-01T00:00:00Z","publication":"2017 Oct","modification":"2026-05-06T00:03:00.154Z","creation":"2019-03-27T02:58:42Z"},"accession":"S-EPMC5636879","cross_references":{"pubmed":["29021522"],"doi":["10.1038/s41467-017-00910-z"]}}