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Updated: May 29, 2026

Sequencing Small Non-coding RNA from Formalin-fixed Tissues and Serum-derived Exosomes from Castration-resistant Prostate Cancer Patients
Published on: November 19, 2019
Integrative genomic, transcriptomic, and RNAi analysis indicates a potential oncogenic role for FAM110B in
Paula Vainio1, Maija Wolf, Henrik Edgren
1Turku Centre for Biotechnology, University of Turku, Turku, Finland.
Background:
Castration-resistant prostate cancer (CRPC) represents a therapeutic challenge for current medications.
Methods:
In order to explore the molecular mechanisms involved in CRPC progression and to identify new therapeutic targets, we analyzed a unique sample set of 11 CRPCs and 7 advanced tumors by array-CGH and gene expression microarrays. The genome-wide DNA and RNA data were integrated to identify genes whose overexpression was driven by their amplification. To assess the functional role of these genes, their expression was analyzed in a transcriptional data set of 329 clinical prostate cancers and the corresponding gene products were silenced using RNA interference in prostate cancer cells.
Results:
Six recurrent genetic targets were identified in the CRPCs; ATP1B1, AR, FAM110B, LAS1L, MYC, and YIPF6. In addition to AR and MYC, FAM110B emerged as a potential key gene involved in CRPC progression in a subset of the tumors. FAM110B was able to regulate AR signaling in prostate cancer cells and FAM110B itself was regulated by androgens. FAM110B siRNA inhibited the growth of prostate cancer cells in vitro, and this effect was substantially enhanced in androgen deficient conditions. Ectopic FAM110B expression in non-cancerous epithelial prostate cells induced aneuploidy and impaired antigen presentation.
Conclusions:
The DNA/RNA gene outlier detection combined with siRNA cell proliferation assay identified FAM110B as a potential growth promoting key gene for CRPC. FAM110B appears to have a key role in the androgen signaling and progression of CRPC impacting multiple cancer hallmarks and therefore highlighting a potential therapeutic target.
Insights
Researchers identified FAM110B as a key gene promoting castration-resistant prostate cancer (CRPC) growth. Silencing FAM110B inhibited cancer cell proliferation, highlighting it as a potential therapeutic target for CRPC.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Castration-resistant prostate cancer (CRPC) presents significant challenges in treatment.
- Current therapeutic options for CRPC are limited, necessitating the identification of novel targets.
Purpose of the Study:
- To investigate the molecular mechanisms underlying CRPC progression.
- To identify novel therapeutic targets for CRPC by analyzing genetic and gene expression data.
Main Methods:
- Utilized array-comparative genomic hybridization (array-CGH) and gene expression microarrays on CRPC and advanced tumor samples.
- Integrated genome-wide DNA and RNA data to pinpoint amplified and overexpressed genes.
- Employed RNA interference (siRNA) to silence candidate genes in prostate cancer cells and assessed functional roles.
Main Results:
- Identified six recurrent genetic targets in CRPC: ATP1B1, AR, FAM110B, LAS1L, MYC, and YIPF6.
- FAM110B was identified as a key gene driving CRPC progression in a subset of tumors, regulating androgen receptor (AR) signaling.
- FAM110B siRNA significantly inhibited prostate cancer cell growth in vitro, particularly under androgen-deficient conditions.
Conclusions:
- FAM110B was identified as a potential growth-promoting gene in CRPC through integrated DNA/RNA analysis and functional assays.
- FAM110B plays a crucial role in androgen signaling and CRPC progression, impacting multiple cancer hallmarks.
- FAM110B represents a promising therapeutic target for castration-resistant prostate cancer.
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