Abstract Oxysterol sulfotransferase (SULT2B) mediates enzymatic sulfation of oxysterols. SULT2B can modulate lipid metabolism by interfering with oxysterol-induced activation of the LXR nuclear receptor, since sulfated oxysterols are LXR inert. Poor survival is linked to reduced SULT2B in primary prostate cancer, and the enzyme is undetectable in clinical metastases of castration resistant prostate cancer (CRPC). SULT2B-null CRPC xenografts show escalated growth while SULT2B-high tumors are growth suppressed, show reduced tumor-emitted bioluminescence and sustain apoptosis. SULT2B silenced cells are more aggressive - evident from EMT-like induction; activated ERK survival signal; and enhanced invasion. To gain mechanistic insight, we probed PC3 CRPC cells for cell-intrinsic and -extrinsic changes due to ectopic SULT2B expression. Results: Single-cell RNA sequences of SULT2B-high PC3 (SA) Part 1 (Regular Abstracts); 2026 Apr 17-22; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2026;86(7 Suppl):Abstract nr 5020.
Park et al. (Fri,) studied this question.