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Updated: Jan 15, 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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Mechanistic Insights Into METTL1/WDR4-Mediated m7G Modification in Prostate Cancer Progression and Its Potential as a
Wangdong Deng1, Shanming Lu2, Guodong Ding1
1Department of Urology, Longgang District Central Hospital of Shenzhen, Shenzhen, Guangdong, China.
Journal of Biochemical and Molecular Toxicology
|October 16, 2025
Summary
N7-methylguanosine (m7G) modification is linked to cancer. This study found that METTL1 and WDR4 are highly expressed in prostate cancer (PCa) and drive cancer cell growth, suggesting they are potential therapeutic targets.
Area of Science:
- Oncology
- Molecular Biology
- Epigenetics
Background:
- N7-methylguanosine (m7G) is a critical RNA modification implicated in oncogenesis.
- The role of m7G modification and its regulators in prostate cancer (PCa) is not well understood.
Purpose of the Study:
- To investigate the function and therapeutic potential of WD repeat domain 4 (WDR4) and methyltransferase like 1 (METTL1) in prostate cancer.
- To explore the regulatory role of METTL1/WDR4 in m7G modification, the PI3K/AKT/mTOR pathway, and oncogenic phenotypes in PCa cells.
Main Methods:
- Quantitative real-time PCR (qRT-PCR) and Western blot for gene and protein expression analysis.
- m7G RNA immunoprecipitation (MeRIP) to assess m7G modification levels.
- Cell proliferation (CCK-8), migration, invasion (Transwell), and apoptosis (TUNEL) assays were performed.
Main Results:
- METTL1 and WDR4 were significantly upregulated in PCa tissues and DU145 cells, correlating with increased m7G levels.
- Knockdown of METTL1/WDR4 reduced DU145 cell proliferation, migration, and invasion, while promoting apoptosis.
- These effects were linked to decreased m7G modification, suppressed PI3K/AKT/mTOR signaling, and downregulation of MYC and VEGF.
Conclusions:
- METTL1 and WDR4 are overexpressed in prostate cancer and contribute to oncogenic phenotypes by regulating m7G modification and the PI3K/AKT/mTOR pathway.
- Targeting METTL1 and WDR4 may offer a novel therapeutic strategy for prostate cancer.
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