ArticleMolecular therapy. Oncology2026
Atorvastatin pre-exposure in hypercholesterolemia remedies 27HC mediated dendritic cell dysfunctions in triple-negative breast cancer.
Article in Molecular therapy. Oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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23 authors.
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Abstract
Early inception of hypercholesterolemia has led to prevalent statin pre-exposure among cancer patients. Furthermore, emerging associations between increased circulating cholesterol, dyslipidemia, and cancer recurrence have spurred the repurposing of statins to combat cancer. However, the mechanistic impact of statin pre-exposure on cancer progression remains unclear. Here, our retrospective study with triple-negative breast cancer (TNBC) patients showed that atorvastatin pre-exposure promotes recurrence-free survival. Atorvastatin pre-exposure in TNBC patients and a preclinical high-fat diet-induced hypercholesterolemic murine tumor model lowered intratumoral 27-hydroxycholesterol (27HC) concentration, as estimated by LC-MS/MS. Within the tumor microenvironment, elevated 27HC interacted with estrogen receptor alpha (ERα) on dendritic cells (DCs), hindering DC maturation, migration, and antigen presentation. Atorvastatin reduced ERα expression on DCs and remediated 27HC-ERα-induced DC dysfunctions, improved DC-mediated T cell priming, thereby facilitating tumor restriction when adoptively transferred to 4T1-bearing NOD/SCID/IL2Rγ
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