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Updated: Apr 24, 2026

Sequencing Small Non-coding RNA from Formalin-fixed Tissues and Serum-derived Exosomes from Castration-resistant Prostate Cancer Patients
12:13

Sequencing Small Non-coding RNA from Formalin-fixed Tissues and Serum-derived Exosomes from Castration-resistant Prostate Cancer Patients

Published on: November 19, 2019

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Whole transcriptome sequencing reveals extensive unspliced mRNA in metastatic castration-resistant prostate cancer

Adam G Sowalsky1, Zheng Xia2, Liguo Wang2

  • 1Division of Hematology and Oncology, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts.

Molecular Cancer Research : MCR
|September 6, 2014
PubMed
Abstract

Insights

Advanced prostate cancer exhibits inefficient RNA splicing, potentially driven by increased transcription or splicing defects. This splicing issue may offer a survival advantage but also presents a vulnerability for targeted therapies.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Metastatic prostate cancer treated with androgen deprivation therapy (ADT) often progresses to castration-resistant prostate cancer (CRPC).
  • Understanding the molecular mechanisms driving CRPC is crucial for developing effective treatments.

Purpose of the Study:

  • To investigate the molecular drivers of castration-resistant prostate cancer (CRPC) using advanced genomic techniques.
  • To identify novel therapeutic vulnerabilities in advanced prostate cancer.

Main Methods:

  • Paired-end RNA sequencing (RNA-seq) was performed on CRPC bone marrow biopsy specimens.
  • Quantitative PCR (qPCR) was used to validate gene expression and splicing patterns.
  • Analysis included identification of gene mutations, fusions, and noncoding RNA expression.

Main Results:

  • Mutations in key prostate cancer genes (e.g., AR, TP53BP1) and a novel SND1:BRAF fusion were identified in CRPC.
  • High expression of noncoding RNAs (ncRNAs) involved in RNA processing, such as MALAT1, was observed.
  • A significant proportion of sequence reads mapped to introns, indicating inefficient mRNA splicing in CRPC specimens compared to normal or early-stage prostate cancer.

Conclusions:

  • Inefficient splicing is a hallmark of advanced prostate cancer, potentially conferring a selective advantage.
  • This splicing defect may impact microRNA networks and represents a potential therapeutic target for CRPC treatment.

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