57 - Finasteride Induces Epigenetic Modulation of Steroid Hormones Biosynthesis and Signaling Pathways

Poster Board Number: 57
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Abstract Body : Cholesterol is a substrate necessary for synthesis of androgens and other steroid hormones. Testosterone is crucial for normal androgen receptor expression, transcription, and translation of molecular proteins necessary for male sexual function and fertility. Finasteride is a drug which inhibits the 5α-reductase enzyme that converts testosterone to the more active dihydrotestosterone. This study focuses on methylation changes associated with genes expressing enzymes and molecular receptors of cholesterol and steroid metabolic pathways following finasteride treatment in human Leydig cells. We identified several genes expressing cholesterol receptors, transport proteins and enzymes in steroid metabolic pathways differentially methylated by finasteride. These include LDLRAD1, LDLRAD4, CAV1 and CAV2, HMGGR and CYP11AI, DEFA1, DEFA3, DEFA1B, AR and UBE3A. There was upregulation of LDLRAD1, LDLRAD4, HMGGR, CAV1 and CAV2 genes. We therefore infer that finasteride, through epigenetic changes, could alter nervous system functions, risk of atherosclerosis and other systems affected by steroid hormone signaling pathways.