S2B). antagonism. Benign cells were insensitive to SR-B1 antagonism, and malignancy collection level of sensitivity inversely correlated with manifestation levels of full-length and splice-variant AR. In androgen-responsive CRPC cell model C4-2, SR-B1 antagonism suppressed cholesterol uptake, de novo steroidogenesis, and AR activity. SR-B1 antagonism also suppressed growth and viability and induced endoplasmic reticulum stress and…