ArticleThe Journal of biological chemistry2018
Loss of dihydrotestosterone-inactivation activity promotes prostate cancer castration resistance detectable by functional imaging.
Article in The Journal of biological chemistry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
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Who cites it
28 citing papers in PubMed, 40 citations in OpenAlex.
- 3beta-HSD1-mediated steroid back-conversion maintains androgen signaling in prostate cancer.Molecular cancer research : MCR · 2026Article
- Article
- Noncanonical functions of UGT2B17 promote castration-resistant prostate cancer progression.The Journal of clinical investigation · 2026Article
- Androgen Effects on Amyloid Precursor Protein Processing Pathways in Cancer: A Systematic Review.Current issues in molecular biology · 2025Review
- A bypass gateway from cholesterol to sex steroid biosynthesis circumnavigates CYP17A1.Nature communications · 2025Article
- CRISPR-Cas-Based Diagnostics in Biomedicine: Principles, Applications, and Future Trajectories.Biosensors · 2025Review
- A novel bone metastasis-related gene signature for predicting prognosis, anti-androgen resistance, and drug choice in prostate cancer.Journal of bone oncology · 2025Article
- An expanded metabolic pathway for androgen production by commensal bacteria.Nature microbiology · 2025Article
- ONECUT2 acts as a lineage plasticity driver in adenocarcinoma as well as neuroendocrine variants of prostate cancer.Nucleic acids research · 2024Article
- Androgen drives melanoma invasiveness and metastatic spread by inducing tumorigenic fucosylation.Nature communications · 2024Article
- MED19 encodes two unique protein isoforms that confer prostate cancer growth under low androgen through distinct gene expression programs.Scientific reports · 2023Article
- ONECUT2 Activates Diverse Resistance Drivers of Androgen Receptor-Independent Heterogeneity in Prostate Cancer.bioRxiv : the preprint server for biology · 2023Article
- Preclinical Imaging of Prostate Cancer.Seminars in nuclear medicine · 2023Review
- Revealing the Role of Alternariol in the Local Steroidogenesis in Human Prostate Normal and Cancer Cells.International journal of molecular sciences · 2023Article
- Cancer-associated fibroblast-secreted glucosamine alters the androgen biosynthesis program in prostate cancer via HSD3B1 upregulation.The Journal of clinical investigation · 2023Article
- BMX controls 3βHSD1 and sex steroid biosynthesis in cancer.The Journal of clinical investigation · 2023Article
- 5-Hydroxyeicosatetraenoic Acid Controls Androgen Reduction in Diverse Types of Human Epithelial Cells.Endocrinology · 2022Article
- Characterization of a castrate-resistant prostate cancer xenograft derived from a patient of West African ancestry.Prostate cancer and prostatic diseases · 2022Article
- Hypoxia-Reoxygenation Couples 3βHSD1 Enzyme and Cofactor Upregulation to Facilitate Androgen Biosynthesis and Hormone Therapy Resistance in Prostate Cancer.Cancer research · 2022Article
- Article
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
Abstract
Androgens such as testosterone and dihydrotestosterone are a critical driver of prostate cancer progression. Cancer resistance to androgen deprivation therapies ensues when tumors engage metabolic processes that produce sustained androgen levels in the tissue. However, the molecular mechanisms involved in this resistance process are unclear, and functional imaging modalities that predict impending resistance are lacking. Here, using the human LNCaP and C4-2 cell line models of prostate cancer, we show that castration treatment-sensitive prostate cancer cells that normally have an intact glucuronidation pathway that rapidly conjugates and inactivates dihydrotestosterone and thereby limits androgen signaling, become glucuronidation deficient and resistant to androgen deprivation. Mechanistically, using CRISPR/Cas9-mediated gene ablation, we found that loss of UDP glucuronosyltransferase family 2 member B15 (UGT2B15) and UGT2B17 is sufficient to restore free dihydrotestosterone, sustained androgen signaling, and development of castration resistance. Furthermore, loss of glucuronidation enzymatic activity was also detectable with a nonsteroid glucuronidation substrate. Of note, glucuronidation-incompetent cells and the resultant loss of intracellular conjugated dihydrotestosterone were detectable
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.