ArticleBritish journal of cancer2025
The long noncoding RNA lncZBTB10 facilitates AR function via S-palmitoylation to promote prostate cancer progression and abiraterone resistance.
Article in British journal of cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Who cites it
5 citing papers in PubMed.
- ZDHHC2-Dependent Palmitoylation Dictates Ferroptosis and Castration Sensitivity in Prostate Cancer via Controlling ACSL4 Degradation and Lipid Peroxidation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Development and Assessment of a Novel Palmitoylation-Related lncRNA Signature for Prognosis and Immune Landscape in Hepatocellular Carcinoma.Oncology research · 2026Article
- Development and validation of a novel palmitoylation-related prognostic signature in head and neck squamous cell carcinoma.Translational cancer research · 2025Article
- Identification of palmitoylation-related lncRNAs as prognostic biomarkers and immune modulators in HCC.Discover oncology · 2025Article
- Integrating Single-Cell and Bulk RNA Sequencing Reveals the Malignant Phenotype of CBX4 in Prostate Cancer.Journal of Cancer · 2025Article
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Authors and funding
9 authors.
Funding
Abstract
backgroundActivation of androgen receptor (AR) by androgen binding to its ligand-binding domain (LBD) has led to the development of clinical drugs that target androgen biosynthesis or the LBD of AR for the treatment of prostate cancer patients. While these drugs initially offer clinical benefits, the emergence of drug resistance is inevitable after a certain duration of treatment.
objectivesExploring alternative AR domains or identifying novel mechanisms for AR activation is crucial for advancing prostate cancer therapies.
methodsA systematic bioinformatic analysis identified novel androgen-responsive long noncoding RNAs (lncRNAs) in prostate cancer, which were verified using loss-of-function and gain-of-function strategies in vitro and in vivo.
resultslncZBTB10 or LINC02986 was overexpressed in prostate cancer specimens and correlated with poor clinical outcomes. Mechanistically, our findings elucidate the pivotal role of lncZBTB10 in facilitating AR function by inducing S-palmitoylation. Moreover, the interaction between lncZBTB10 and AR not only fosters but also orchestrates biomolecular condensates within the nucleus driven by a novel RNA-binding domain, particularly in prostate cancer cells. Notably, the overexpression of lncZBTB10 not only promotes tumor growth in vivo but also triggers abiraterone resistance in vitro by inducing AR expression.
conclusionsThese results collectively reveal a novel mechanism by which lncZBTB10 regulates AR function in prostate cancer cells.
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