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Induction of Invasive Transitional Cell Bladder Carcinoma in Immune Intact Human MUC1 Transgenic Mice: A Model for Immunotherapy Development
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Bladder Cancer Growth is Inhibited by Upregulating CircFUT8 through the METTL14/FMR1 Signaling Pathway.

Weifeng Yang1,2, Jinhui Zha3, Youjuan Tang4

  • 1Department of Urology, Qianhai Shekou Free Trade Zone Hospital, Shenzhen, China. weifeng.yang@uszh.org.cn.

Cell Biochemistry and Biophysics
|June 10, 2025
PubMed
Summary

This study reveals that the METTL14/FMR1 signaling pathway enhances circFUT8 expression, inhibiting bladder cancer (BCa) cell growth and migration. CircFUT8 emerges as a potential therapeutic target for BCa.

Keywords:
Bladder cancerCircFUT8FMR1M6AMETTL14

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Area of Science:

  • Oncology
  • Molecular Biology
  • Epigenetics

Background:

  • Bladder cancer (BCa) is a prevalent malignancy globally.
  • Understanding the molecular mechanisms driving BCa progression is crucial for developing effective therapies.

Purpose of the Study:

  • To investigate the role of the N6-methyladenosine (m6A)/circRNA regulatory axis in BCa.
  • To elucidate the underlying molecular mechanisms involving circFUT8, METTL14, and FMR1 in BCa.

Main Methods:

  • Analysis of 15 paired BCa and adjacent non-tumor tissues.
  • Cellular experiments involving gene overexpression and knockdown (METTL14, circFUT8, FMR1).
  • RNA immunoprecipitation (RIP) assays and in vivo mouse models.

Main Results:

  • CircFUT8 expression was downregulated in BCa tissues and correlated positively with METTL14 levels.
  • METTL14 overexpression upregulated circFUT8, while circFUT8 silencing counteracted METTL14's effects on BCa cells.
  • FMR1 interacted with circFUT8, with FMR1 overexpression enhancing circFUT8 levels and inhibiting tumor growth in mice.

Conclusions:

  • The METTL14/FMR1 signaling axis promotes circFUT8 expression, thereby inhibiting BCa cell growth and migration.
  • CircFUT8 represents a promising therapeutic target for bladder cancer.
  • This study provides novel insights into the epigenetic regulation of BCa progression.