ArticleMolecular cancer research : MCR2015
Whole transcriptome sequencing reveals extensive unspliced mRNA in metastatic castration-resistant prostate cancer.
Article in Molecular cancer research : MCR, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
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Who cites it
59 citing papers in PubMed, 105 citations in OpenAlex.
- SND1 regulates the androgen signaling axis by stabilizing EIF3B mRNA to facilitate the deterioration of prostate cancer.Molecular genetics and genomics : MGG · 2026Article
- SETD7 Dual Role in Disease and Opportunities for Therapeutic Intervention: Current Perspectives.Journal of inflammation research · 2025Review
- Unveiling novel double-negative prostate cancer subtypes through single-cell RNA sequencing analysis.NPJ precision oncology · 2024Article
- Predicting prostate cancer progression with a Multi-lncRNA expression-based risk score and nomogram integrating ISUP grading.Non-coding RNA research · 2024Article
- Unveiling Novel Double-Negative Prostate Cancer Subtypes Through Single-Cell RNA Sequencing Analysis.bioRxiv : the preprint server for biology · 2024Article
- Defining Biological and Biochemical Functions of Noncanonical SET Domain Proteins.Journal of molecular biology · 2024Review
- Beyond the Genome: Deciphering the Role of MALAT1 in Breast Cancer Progression.Current genomics · 2024Review
- MALAT1 promotes FOXA1 degradation by competitively binding to miR-216a-5p and enhancing neuroendocrine differentiation in prostate cancer.Translational oncology · 2024Article
- LncRNA MALAT1 signaling pathway and clinical applications in overcome on cancers metastasis.Clinical and experimental medicine · 2023Review
- Structure, activity and function of the lysine methyltransferase SETD5.Frontiers in endocrinology · 2023Review
- H3 histone methylation landscape in male urogenital cancers: from molecular mechanisms to epigenetic biomarkers and therapeutic targets.Frontiers in cell and developmental biology · 2023Review
- Downregulation of SETD5 Suppresses the Tumorigenicity of Hepatocellular Carcinoma Cells.Molecules and cells · 2022Article
- Assessment of Androgen Receptor Splice Variant-7 as a Biomarker of Clinical Response in Castration-Sensitive Prostate Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022Article
- Understanding and targeting prostate cancer cell heterogeneity and plasticity.Seminars in cancer biology · 2022Review
- Overarching roles of diacylglycerol signaling in cancer development and antitumor immunity.Science signaling · 2022Review
- A Systematic Review to Define the Multi-Faceted Role of Lysine Methyltransferase SETD7 in Cancer.Cancers · 2022Review
- MALAT1 Fusions and Basal Cells Contribute to Primary Resistance against Androgen Receptor Inhibition in TRAMP Mice.Cancers · 2022Article
- Analysis on the interactions between the first introns and other introns in mitochondrial ribosomal protein genes.Frontiers in microbiology · 2022Article
- Regulation of Neuroendocrine-like Differentiation in Prostate Cancer by Non-Coding RNAs.Non-coding RNA · 2021Review
- Alternative polyadenylation: An untapped source for prostate cancer biomarkers and therapeutic targets?Asian journal of urology · 2021Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
unlabelledMen with metastatic prostate cancer who are treated with androgen deprivation therapies (ADT) usually relapse within 2 to 3 years with disease that is termed castration-resistant prostate cancer (CRPC). To identify the mechanism that drives these advanced tumors, paired-end RNA-sequencing (RNA-seq) was performed on a panel of CRPC bone marrow biopsy specimens. From this genome-wide approach, mutations were found in a series of genes with prostate cancer relevance, including AR, NCOR1, KDM3A, KDM4A, CHD1, SETD5, SETD7, INPP4B, RASGRP3, RASA1, TP53BP1, and CDH1, and a novel SND1:BRAF gene fusion. Among the most highly expressed transcripts were 10 noncoding RNAs (ncRNAs), including MALAT1 and PABPC1, which are involved in RNA processing. Notably, a high percentage of sequence reads mapped to introns, which were determined to be the result of incomplete splicing at canonical splice junctions. Using quantitative PCR (qPCR), a series of genes (AR, KLK2, KLK3, STEAP2, CPSF6, and CDK19) were confirmed to have a greater proportion of unspliced RNA in CRPC specimens than in normal prostate epithelium, untreated primary prostate cancer, and cultured prostate cancer cells. This inefficient coupling of transcription and mRNA splicing suggests an overall increase in transcription or defect in splicing. IMPLICATIONS: Inefficient splicing in advanced prostate cancer provides a selective advantage through effects on microRNA networks but may render tumors vulnerable to agents that suppress rate-limiting steps in splicing.
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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.