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December 8, 2025Journal of Clinical InvestigationOpen Access

Non-canonical functions of UGT2B17 promote castrate-resistant prostate cancer progression

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Authors

SKSonia H.Y. KungJQJianfei QiXDXuesen Dong

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Overview

Laboratory findings demonstrate targeting UGT2B17 reduces tumor growth in therapy-resistant prostate cancer models, suggesting it as a therapeutic target.

Key Points

  • Investigate the role of UGT2B17 in therapy-resistant prostate cancer and its potential as a therapeutic target.
  • Examined UGT2B17 functions in advanced prostate tumors.
  • Used inhibitors to target UGT2B17 in therapy-resistant tumor models.
  • Analyzed effects on cell division and DNA damage response.
  • UGT2B17 promotes tumor progression independent of androgen catabolism.
  • Targeting UGT2B17 with inhibitors reduces tumor growth in therapy-resistant models.
  • UGT2B17 is involved in regulating cell division and DNA damage response.

Cite This Study

Kung et al. (2025) studied this question.

synapsesocial.com/papers/693624ce4fa91c937236ceabhttps://doi.org/10.1172/jci196495
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Also Consider

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  1. 1Roles of Uridine Diphosphoglucuronosyltransferase 2B Enzymes in Cancer Susceptibility and Treatment: A Review2026
  2. 2Downregulation of UGT2B15 and UGT2B17 contributes to acquired androgen antagonist resistance in prostate cancer cells2024
  3. 3UGT2B15 Acts as a Critical Detoxification Barrier Against Chemi-Cal-Induced Hepatotoxicity and Carcinogenesis via the Androgen Receptor Axis2026
  4. 4Non-canonical transcriptional regulation of the poor prognostic factor UGT2B17 in chronic lymphocytic leukemic and normal B cells2024
  5. 5The Dual Role of Human UDP-Glucuronosyltransferase-Mediated Metabolism in Tumor Drug Resistance: Mechanisms and Prospects2026