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Updated: May 6, 2026

An Orthotopic Bladder Cancer Model for Gene Delivery Studies
Published on: December 1, 2013
FTO promotes bladder cancer progression and stemness-associated phenotypes.
1Department of Breast Surgery, The Third Affiliated Hospital of Soochow University, 185 Juqian Street, Changzhou, 213003 Jiangsu People's Republic of China.
The fat mass and obesity-associated protein (FTO) is overexpressed in bladder cancer, promoting tumor growth and spread. Inhibiting FTO may offer a new therapeutic strategy for bladder cancer patients.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- The fat mass and obesity-associated protein (FTO) is an m6A demethylase implicated in various cancers.
- Its role in bladder cancer (BCa) progression and stemness remains largely unexplored.
Purpose of the Study:
- To investigate the expression and functional significance of FTO in bladder cancer.
- To explore FTO's impact on bladder cancer cell proliferation, migration, invasion, and stemness.
Main Methods:
- Analysis of The Cancer Genome Atlas (TCGA) data and validation in BCa cell lines.
- In vitro functional assays (cell proliferation, migration, invasion, colony formation) and in vivo xenograft models.
- Transcriptomic analysis to identify associated molecular pathways.
Main Results:
- FTO is significantly overexpressed in bladder cancer tissues and linked to poorer survival.
- FTO knockdown suppressed BCa cell proliferation, migration, invasion, and colony formation in vitro.
- FTO depletion inhibited tumor growth and liver colonization in vivo, and was associated with EMT and CSC pathways.
Conclusions:
- FTO acts as an oncoprotein in bladder cancer, driving progression and stemness.
- FTO inhibition impairs bladder cancer growth and metastasis.
- FTO represents a potential therapeutic target and prognostic marker for bladder cancer.
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