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Updated: Jan 10, 2026

Identification of Transcription Factor Regulators using Medium-Throughput Screening of Arrayed Libraries and a Dual-Luciferase-Based Reporter
Published on: March 27, 2020
FGF12 Enhances Prostate Cancer Cell Survival via the YB1-lncRNA Axis.
Zechao Huang1, Sonia H Y Kung1, Hans Adomat1
1The Vancouver Prostate Centre, Vancouver General Hospital, 2660 Oak Street, Vancouver, BC V6H 3Z6, Canada.
Fibroblast growth factor 12 (FGF12) drives aggressive neuroendocrine prostate cancer by stabilizing oncogenic RNAs. Targeting the FGF12-YB1-lncRNA pathway offers new therapeutic strategies for this therapy-resistant cancer.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Treatment-induced neuroendocrine prostate cancer (t-NEPC) is an aggressive, therapy-resistant subtype of prostate cancer.
- Lineage plasticity and poor response to standard therapies characterize t-NEPC.
- Post-transcriptional regulation's role in t-NEPC is less understood than transcriptional mechanisms.
Purpose of the Study:
- To identify novel post-transcriptional regulators of t-NEPC.
- To elucidate the molecular mechanisms driving t-NEPC progression.
- To explore potential therapeutic targets for t-NEPC.
Main Methods:
- Transcriptomic analysis of patient biopsies, xenografts, and cell models.
- Immunohistochemistry validation in archival specimens.
- Functional assays, RNA sequencing, and affinity purification-mass spectrometry.
Main Results:
- Fibroblast growth factor 12 (FGF12) expression is significantly elevated in t-NEPC.
- FGF12 promotes cancer cell survival against chemotherapeutic agents.
- FGF12 interacts with Y-box binding protein 1 (YB1) to stabilize oncogenic long noncoding RNAs (NEAT1, MALAT1).
Conclusions:
- A novel FGF12-YB1-lncRNA signaling axis drives t-NEPC progression.
- This pathway represents a potential therapeutic target for aggressive prostate cancer.
- Understanding post-transcriptional regulation is crucial for t-NEPC treatment strategies.
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