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Updated: Feb 22, 2026
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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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LSD1-Mediated Epigenetic Reprogramming Drives CENPE Expression and Prostate Cancer Progression
Yi Liang1, Musaddeque Ahmed1, Haiyang Guo1
1Princess Margaret Cancer Centre/University Health Network, Toronto, Ontario, Canada.
Cancer Research
|September 17, 2017
Summary
Chromatin modifier LSD1 reprogramming drives castration-resistant prostate cancer (CRPC) by activating cell-cycle genes like CENPE. Targeting CENPE significantly reduces tumor growth, offering a new therapeutic strategy for CRPC.
Area of Science:
- Oncology
- Epigenetics
- Molecular Biology
Background:
- Androgen receptor (AR) signaling drives prostate cancer.
- Androgen-deprivation therapy (ADT) is a standard treatment but leads to castration-resistant prostate cancer (CRPC).
- The chromatin modifier LSD1 regulates AR activity.
Purpose of the Study:
- Investigate epigenetic reprogramming of LSD1 in CRPC.
- Identify genes regulated by LSD1 in CRPC.
- Determine the therapeutic potential of targeting LSD1-regulated genes.
Main Methods:
- Analysis of LSD1 epigenetic reprogramming in CRPC models.
- Identification of LSD1 and AR co-binding targets.
- Genetic deletion and pharmacological inhibition of CENPE.
Main Results:
- LSD1 undergoes epigenetic reprogramming in CRPC.
- Reprogramming activates cell-cycle genes, including CENPE, via LSD1 and AR co-binding.
- Loss of RB1 is associated with CENPE regulation in CRPC.
- CENPE inhibition significantly decreases CRPC tumor growth.
Conclusions:
- LSD1-mediated epigenetic reprogramming drives CRPC progression.
- CENPE is a key driver of CRPC growth.
- Targeting CENPE offers a promising therapeutic strategy for CRPC.
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