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Updated: Jun 22, 2025

Author Spotlight: Tracing the Ferroptotic Signatures and Cell Death Dynamics in Medulloblastoma for Advanced Therapeutics
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Author Spotlight: Tracing the Ferroptotic Signatures and Cell Death Dynamics in Medulloblastoma for Advanced Therapeutics

Published on: March 15, 2024

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Pro-oncogene FBI-1 inhibits the ferroptosis of prostate carcinoma PC-3 cells via the microRNA-324-3p/GPX4 axis

Mingsheng Liu1, Chenxiang Xu1, Hua Yang2

  • 1Second Ward of Urology, Qujing Affiliated Hospital of Kunming Medical University, Qujing City 655000, Yunnan Province, People's Republic of China.

Journal of Cancer
|July 1, 2024
PubMed

Insights

Factor that binds to inducer of short transcripts-1 (FBI-1) inhibits ferroptosis in prostate cancer by regulating the miR-324-3p/glutathione peroxidase 4 (GPX4) axis. This finding offers a new therapeutic target for endocrine-independent prostate carcinoma.

Area of Science:

  • Oncology
  • Cell Death Mechanisms
  • Molecular Biology

Background:

  • Ferroptosis, a non-apoptotic programmed cell death, presents a novel antitumor strategy.
  • The proto-oncogene FBI-1 is implicated in malignancies and therapy resistance.
  • The role of FBI-1 in endocrine-independent prostate carcinoma ferroptosis remains unelucidated.

Purpose of the Study:

  • To investigate the role of FBI-1 in ferroptosis of endocrine-independent prostate carcinoma.
  • To elucidate the molecular mechanisms underlying FBI-1-mediated ferroptosis.
  • To identify potential therapeutic targets for prostate cancer treatment.

Main Methods:

  • Utilized PC-3 cell line, a model for endocrine-independent prostate carcinoma.
  • Investigated the expression levels of FBI-1, miR-324-3p, and GPX4.
  • Employed overexpression and knockdown techniques for FBI-1.
  • Analyzed the regulatory relationship between FBI-1, miR-324-3p, and GPX4.
  • Examined clinical specimens for correlation analysis.

Main Results:

  • FBI-1 overexpression inhibited ferroptosis by increasing GPX4 levels.
  • FBI-1 knockdown induced ferroptosis by decreasing GPX4 levels.
  • miR-324-3p targets GPX4, leading to ferroptosis.
  • FBI-1 represses miR-324-3p expression via SP1 inhibition.
  • Clinical data showed positive correlation between FBI-1 and GPX4, and negative correlation between FBI-1 and miR-324-3p.

Conclusions:

  • FBI-1 inhibits ferroptosis in prostate carcinoma PC-3 cells through the miR-324-3p/GPX4 axis.
  • FBI-1 upregulates GPX4 by downregulating miR-324-3p, thereby suppressing ferroptosis.
  • The FBI-1/miR-324-3p/GPX4 pathway represents a potential therapeutic target for endocrine-independent prostate carcinoma.
Keywords:
factor that binds to the inducer of short transcripts-1glutathione peroxidase 4miRNA-324-3p

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