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Updated: Jun 10, 2026
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3-D Cell Culture System for Studying Invasion and Evaluating Therapeutics in Bladder Cancer
Published on: September 13, 2018
EP300 promotes bladder cancer cell migration through SNAI2
Qing Zhang1,2, Chongjie He1, Yingzhou Hong1
1Yunnan Key Laboratory of Cell Metabolism and Disease, Center for Life Sciences, School of Life Sciences, Yunnan University, Kunming, China.
Plos One
|June 8, 2026
Summary
EP300 promotes bladder cancer invasion by upregulating SNAI2. Targeting EP300 with A485 inhibits cancer cell migration and invasion, suggesting a potential therapeutic strategy for bladder cancer.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- EP300, a transcriptional coactivator, is frequently mutated in bladder cancer and correlates with malignancy.
- Muscle-invasive progression in aggressive bladder cancers is linked to epithelial-mesenchymal transition (EMT).
Purpose of the Study:
- To validate the association between EP300 and bladder cancer malignancy.
- To investigate the therapeutic potential of EP300 inhibition using A485 in bladder cancer models.
Main Methods:
- Immunohistochemical staining of bladder cancer tissues.
- In vitro assays (scratch wound healing, Transwell) using bladder cancer cell lines (SW780, T24, RT4, 5637).
- 3D organoid culture, in vivo mouse models, Bulk RNAseq, and Western blotting.
Main Results:
- A485 significantly inhibited bladder cancer cell migration and disrupted organoid structures.
- A485 showed a trend toward inhibiting in vivo bladder cancer invasion.
- A485 downregulated SNAI2 signaling and reduced H3K27ac levels, while SNAI2 overexpression enhanced cell migration.
Conclusions:
- EP300 promotes bladder cancer cell migration and invasion by upregulating SNAI2.
- Targeting EP300 with A485 is a potential therapeutic strategy to inhibit bladder cancer invasion.
