Cholesterol and lipid metabolism dysregulation in prostate cancer: targeting endoplasmic reticulum-mitochondria contact sites

Prostate cancer (PCa) is a leading cause of cancer-related deaths in men, with treatment-resistant forms posing significant clinical challenges. Androgen receptor (AR) signaling is central to PCa progression is. This study focuses on the role of ER-mitochondria contact sites (MERCs) in prostate cancer cells. Hypothesis is that MERCs are central to AR activation and treatment resistance, as they regulate steroid hormone synthesis, mitochondrial dynamics, and apoptosis. By using variety of PCa cell models, we can study how MERCs are regulated and how they affect cell behavior in different biological and cancer-typical environments. We aim to identify key regulators of MERC pathways, the mechanisms of regulation, and investigate whether different drugs affect the behavior of cancer cells via MERCs. By increasing knowledge on MERCs, we seek to develop innovative strategies for overcoming treatment resistance and improving PCa outcomes.