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Tumor-Suppressive and Immune-Stimulating Roles of Cholesterol 25-hydroxylase in Pancreatic Cancer Cells
Journal article   Peer reviewed

Tumor-Suppressive and Immune-Stimulating Roles of Cholesterol 25-hydroxylase in Pancreatic Cancer Cells

Noreen McBrearty, Christina Cho, Jinyun Chen, Farima Zahedi, Amy R Peck, Enrico Radaelli, Charles-Antoine Assenmacher, Clarice Pavlak, Anne Devine, Pengfei Yu, …
Molecular cancer research, Vol.21(3), pp.228-239
03/01/2023
DOI: 10.1158/1541-7786.MCR-22-0602
PMCID: PMC9992122
PMID: 36378658
url
https://pmc.ncbi.nlm.nih.gov/articles/PMC9992122/pdf/nihms-1852574.pdfView
Open Access

Abstract

Cholesterol dependence is an essential characteristic of pancreatic ductal adenocarcinoma (PDAC). Cholesterol 25-hydroxylase (CH25H) catalyzes monooxygenation of cholesterol into 25-hydroxycholesterol, which is implicated in inhibiting cholesterol biosynthesis and in cholesterol depletion. Here, we show that, within PDAC cells, accumulation of cholesterol was facilitated by the loss of CH25H. Methylation of the CH25H gene and decreased levels of CH25H expression occurred in human pancreatic cancers and was associated with poor prognosis. Knockout of Ch25h in mice accelerated progression of Kras-driven pancreatic intraepithelial neoplasia. Conversely, restoration of CH25H expression in human and mouse PDAC cells decreased their viability under conditions of cholesterol deficit, and decelerated tumor growth in immune competent hosts. Mechanistically, the loss of CH25H promoted autophagy resulting in downregulation of MHC-I and decreased CD8+ T-cell tumor infiltration. Re-expression of CH25H in PDAC cells combined with immune checkpoint inhibitors notably inhibited tumor growth. We discuss additional benefits that PDAC cells might gain from inactivation of CH25H and the potential translational importance of these findings for therapeutic approaches to PDAC. Loss of CH25H by pancreatic cancer cells may stimulate tumor progression and interfere with immunotherapies.
Animals Carcinoma, Pancreatic Ductal - pathology Humans Mice Mice, Knockout Pancreatic Neoplasms Pancreatic Neoplasms - pathology Steroid Hydroxylases - metabolism

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