ArticleOncogene2020
Systematic characterization of chromatin modifying enzymes identifies KDM3B as a critical regulator in castration resistant prostate cancer.
Article in Oncogene, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 45 citations in OpenAlex.
- Targeting KDM3B Elicits Anti-tumor Immunity by Alleviating SHP1-mediated STING Suppression in Triple-Negative Breast Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- ANP32E drives lung adenocarcinoma progression via GSK3β-mediated glycolytic reprogramming.Cell death & disease · 2026Article
- Metabolomics using anion-exchange chromatography mass spectrometry for the analysis of cells, tissues and biofluids.Nature protocols · 2026Review
- KDM3B Predicts Expression Signature, Prognosis Value, and Immune Characteristics of Cancers: A Pan-Cancer Analysis.BioMed research international · 2026Article
- KDM3B promotes neural invasion in colorectal cancer through TrkA upregulation by inhibiting H3K9 dimethylation.iScience · 2025Article
- Characterizing epithelial-mesenchymal transition-linked heterogeneity in breast cancer circulating tumor cells at a single-cell level.Molecular oncology · 2025Article
- KDM3B suppresses castration-resistance prostate cancer cell proliferation by promoting PTEN expression.European journal of medical research · 2025Article
- Coregulators determine androgen receptor activity in prostate cancer.Bioscience reports · 2025Review
- Prostate cancer epigenetics - from pathophysiology to clinical application.Nature reviews. Urology · 2025Review
- Histone-modifying enzymes as drivers and therapeutic targets in androgen-resistant prostate cancer.Frontiers in endocrinology · 2025Review
- [Advances in the application of ion chromatography-mass spectrometry in the fields of life and health].Se pu = Chinese journal of chromatography · 2024Review
- Epigenetic roles of KDM3B and KDM3C in tumorigenesis and their therapeutic implications.Cell death & disease · 2024Review
- Molecular landscape for risk prediction and personalized therapeutics of castration-resistant prostate cancer: at a glance.Frontiers in endocrinology · 2024Review
- Histone lysine demethylase 3B regulates autophagy via transcriptional regulation ofInternational journal of oncology · 2023Article
- Comprehensive Analyses of Prognostic Values and Immune Infiltration of KDM3 Gene Family in Hepatocellular Carcinoma.Molecular biotechnology · 2023Article
- Ion-Exchange Chromatography Coupled to Mass Spectrometry in Life Science, Environmental, and Medical Research.Analytical chemistry · 2023Review
- Epigenetic (De)regulation in Prostate Cancer.Cancer treatment and research · 2023Article
- Novel forms of prostate cancer chemoresistance to successful androgen deprivation therapy demand new approaches: Rationale for targeting BET proteins.The Prostate · 2022Review
- Epigenetic Editing in Prostate Cancer: Challenges and Opportunities.Epigenetics · 2022Review
- Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 3 countries.
Funding
Abstract
Androgen deprivation therapy (ADT) is the standard care for prostate cancer (PCa) patients who fail surgery or radiotherapy. While initially effective, the cancer almost always recurs as a more aggressive castration resistant prostate cancer (CRPC). Previous studies have demonstrated that chromatin modifying enzymes can play a critical role in the conversion to CRPC. However, only a handful of these potential pharmacological targets have been tested. Therefore, in this study, we conducted a focused shRNA screen of chromatin modifying enzymes previously shown to be involved in cellular differentiation. We found that altering the balance between histone methylation and demethylation impacted growth and proliferation. Of all genes tested, KDM3B, a histone H3K9 demethylase, was found to have the most antiproliferative effect. These results were phenocopied with a KDM3B CRISPR/Cas9 knockout. When tested in several PCa cell lines, the decrease in proliferation was remarkably specific to androgen-independent cells. Genetic rescue experiments showed that only the enzymatically active KDM3B could recover the phenotype. Surprisingly, despite the decreased proliferation of androgen-independent cell no alterations in the cell cycle distribution were observed following KDM3B knockdown. Whole transcriptome analyses revealed changes in the gene expression profile following loss of KDM3B, including downregulation of metabolic enzymes such as ARG2 and RDH11. Metabolomic analysis of KDM3B knockout showed a decrease in several critical amino acids. Overall, our work reveals, for the first time, the specificity and the dependence of KDM3B in CRPC proliferation.
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Registered trials
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