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Updated: Aug 30, 2025

Author Spotlight: Tracing the Ferroptotic Signatures and Cell Death Dynamics in Medulloblastoma for Advanced Therapeutics
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mRNA-Modified FUS/NRF2 Signalling Inhibits Ferroptosis and Promotes Prostate Cancer Growth

Ning Wang1, Ying Yu2, Rongjiang Wang1

  • 1Department of Urology, The First People's Hospital Affiliated to Huzhou Normal College, Huzhou 313000, China.

Computational and Mathematical Methods in Medicine
|August 29, 2022
PubMed
Abstract

Insights

FUS protein and m6A modification promote prostate adenocarcinoma (PRAD) growth by inhibiting ferroptosis. Targeting this pathway could offer new therapeutic strategies for PRAD.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Prostate adenocarcinoma (PRAD) progression is not fully understood.
  • The roles of FUS protein and mRNA modifications in PRAD are under investigation.
  • Ferroptosis is a key mechanism in cancer development.

Purpose of the Study:

  • To investigate the role of FUS/NRF2 signaling in PRAD.
  • To explore the impact of mRNA modification on ferroptosis in PRAD.
  • To identify potential therapeutic targets for PRAD.

Main Methods:

  • Bioinformatics analysis of FUS expression and m6A modification in PRAD.
  • Detection of ferroptosis, apoptosis, and autophagy markers in prostate cancer cells (CRPC).
  • Assessment of oxidative stress and NRF2/HO-1 pathway indicators.

Main Results:

  • High FUS expression in PRAD correlates with reduced patient survival.
  • FUS knockdown decreased m6A methylation, P53, and GPX4, while activating the NRF2/HO-1 pathway.
  • Reduced FUS expression promoted ferroptosis, inhibiting PRAD growth.

Conclusions:

  • FUS and m6A modification promote PRAD growth by inhibiting ferroptosis.
  • Increased m6A modification enhances FUS expression, leading to PRAD growth.
  • Targeting FUS/NRF2 signaling and m6A modification may be a therapeutic strategy for PRAD.

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