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The study examines the dual role of oxysterol sulfotransferase (SULT2B) in inhibiting prostate cancer through its effects on cellular metabolism and immune response.

April 5, 2026Cancer Research0 citations

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Abstract 5020: Oxysterol sulfotransferase in prostate cancer inhibition: Cell-intrinsic and -extrinsic roles

BPBobae ParkThe University of Texas Health Science Center at San Antonio ZZZZ Zhao ZhangTianjin University of Science and Technology CWChiou-Miin WangThe University of Texas Health Science Center at San Antonio

Key Points

The study examines the dual role of oxysterol sulfotransferase (SULT2B) in inhibiting prostate cancer through its effects on cellular metabolism and immune response.
Utilized SULT2B-null and SULT2B-high xenograft models of castration resistant prostate cancer (CRPC).
Conducted single-cell RNA sequencing to analyze gene expression changes.
Employed bioinformatics to probe changes in prostate cancer cell traits.
Performed RT-qPCR to confirm molecular changes.
Used multiplex immunofluorescence for visualizing immune cell interactions.
SULT2B-high tumors exhibited reduced growth and increased apoptosis compared to SULT2B-null tumors.
Gene expression analysis revealed a transition from mesenchymal to epithelial traits in SULT2B-high cells.
Notable downregulation of key genes associated with lethal CRPC, including FOXA2 and MMP16, in SULT2B-high cells.
MΦ dynamics were altered, with M1MΦ present in SULT2B-high xenografts while M2MΦ were found in SULT2B-silenced models.
AKR1C3 expression was elevated in SULT2B-silenced cells, linking oxysterol signaling to androgen metabolism.

Abstract

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.

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Cite This Study

Park et al. (Fri,) studied this question.

synapsesocial.com/papers/69d1fd29a79560c99a0a2fd0 https://doi.org/https://doi.org/10.1158/1538-7445.am2026-5020

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