Related Experiment Video

Updated: Apr 15, 2026

SUMO-Binding Entities SUBEs as Tools for the Enrichment, Isolation, Identification, and Characterization of the SUMO Proteome in Liver Cancer
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SUMO-Binding Entities SUBEs as Tools for the Enrichment, Isolation, Identification, and Characterization of the SUMO Proteome in Liver Cancer

Published on: November 1, 2019

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TRIM28 orchestrates SUMO-ubiquitin crosstalk to stabilize PPARG and drive bladder cancer progression

Xuefeng Fan1, Zexuan Li1, Qiongqiong Gao1

  • 1Department of Urology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China.

Cell Death & Disease
|April 13, 2026
PubMed

Insights

Tripartite Motif 28 (TRIM28) promotes bladder cancer (BLCA) by stabilizing PPARG, enhancing cholesterol metabolism, and driving tumor growth. Targeting TRIM28 offers a potential therapeutic strategy for metabolic intervention in BLCA.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Bladder cancer (BLCA) presents a significant health challenge with increasing incidence and few treatment options.
  • The role of the Tripartite Motif (TRIM) gene family in BLCA pathogenesis requires further elucidation.

Purpose of the Study:

  • To investigate the function of the TRIM family in BLCA.
  • To identify specific TRIM members involved in BLCA progression and their underlying mechanisms.

Main Methods:

  • Integrated multi-cohort transcriptomic analyses of BLCA.
  • Functional validation including gene depletion and overexpression studies.
  • Mechanistic studies involving protein binding assays, SUMOylation, and ubiquitination analyses.

Main Results:

  • TRIM28 was the most upregulated TRIM gene in BLCA, correlating with poor prognosis.
  • TRIM28 depletion inhibited BLCA cell proliferation; overexpression enhanced it.
  • TRIM28 SUMOylates PPARG, inhibiting its degradation and stabilizing the protein.
  • Stabilized PPARG activates cholesterol biosynthesis genes (DHCR7, DHCR24), promoting BLCA progression.

Conclusions:

  • A novel TRIM28-PPARG SUMO-ubiquitin crosstalk axis drives metabolic reprogramming and tumor growth in BLCA.
  • TRIM28-mediated PPARG SUMOylation represents a potential therapeutic target for metabolic interventions in bladder cancer.

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