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Updated: Jul 7, 2025

Induction of Invasive Transitional Cell Bladder Carcinoma in Immune Intact Human MUC1 Transgenic Mice: A Model for Immunotherapy Development
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Induction of Invasive Transitional Cell Bladder Carcinoma in Immune Intact Human MUC1 Transgenic Mice: A Model for Immunotherapy Development

Published on: October 30, 2013

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TRAIP suppresses bladder cancer progression by catalyzing K48-linked polyubiquitination of MYC

Jingtian Yu1, Mingxing Li1, Lingao Ju2

  • 1Department of Urology, Laboratory of Precision Medicine, Zhongnan Hospital of Wuhan University, Wuhan, China.

Oncogene
|December 20, 2023
PubMed

Insights

TRAF-interacting protein (TRAIP) suppresses bladder cancer (BLCA) by degrading the MYC protein. Reduced TRAIP expression correlates with poor BLCA prognosis, highlighting its role in cancer progression.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • TRAF-interacting protein (TRAIP) is an E3 ligase crucial for genome integrity and cancer.
  • Reduced TRAIP expression is observed in bladder cancer (BLCA) and linked to poor prognosis.

Purpose of the Study:

  • To investigate the role of TRAIP in BLCA progression.
  • To identify TRAIP's molecular targets and mechanisms in BLCA.

Main Methods:

  • In vitro and in vivo experiments were conducted using BLCA cells.
  • Ubiquitination assays, Western blotting, and cell proliferation/migration assays were performed.
  • MYC expression and transcriptional activity were analyzed.

Main Results:

  • TRAIP inhibits BLCA cell proliferation and migration.
  • TRAIP directly targets MYC, promoting its K48-linked polyubiquitination and proteasomal degradation.
  • MYC downregulation by TRAIP impedes BLCA progression, and restoring MYC reverses these effects.
  • A negative feedback loop exists where MYC may regulate TRAIP transcription.

Conclusions:

  • TRAIP acts as a tumor suppressor in BLCA by degrading MYC.
  • The TRAIP-MYC axis represents a potential therapeutic target for bladder cancer.
  • Understanding this regulatory feedback loop is key to developing novel BLCA treatments.

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