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USP7 stabilizes EZH2 and enhances cancer malignant progression
Nana Zheng1,2, Man Chu1, Min Lin1
1Department of Obstetrics and Gynecology, The Second Affiliated Hospital of Wenzhou Medical University Wenzhou 325027, Zhejiang Province, China.
American Journal of Cancer Research
|February 18, 2020
Summary
The study reveals that USP7 deubiquitinates and stabilizes EZH2, promoting cancer cell growth and invasion. Targeting the USP7/EZH2 pathway offers a potential new therapeutic strategy for cancer treatment.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Enhancer of Zeste Homolog 2 (EZH2) is a histone methyltransferase crucial for tumor progression by regulating progenitor genes.
- The precise molecular mechanisms governing EZH2's role in cancer malignancy are not fully understood.
Purpose of the Study:
- To investigate the regulatory mechanisms of EZH2 in human cancers.
- To elucidate the deubiquitination pathway controlling EZH2 stability and function.
Main Methods:
- Co-immunoprecipitation (Co-IP)
- Transfection and gene knockdown studies (RT-PCR, Western blotting)
- Cellular assays (Transwell assays for invasion and migration)
- In vivo studies using mouse models
Main Results:
- Usprotein 7 (USP7) was identified as a key regulator of EZH2 in human cancer cells and in vivo.
- USP7 overexpression increased EZH2 protein levels and promoted cancer cell growth and invasion through EZH2 deubiquitination.
- USP7 knockdown decreased EZH2 levels, inhibiting cancer cell migration, invasion, and tumor growth in mice.
Conclusions:
- USP7 deubiquitinates and stabilizes EZH2, thereby promoting cancer progression.
- The USP7/EZH2 axis represents a potential therapeutic target for human cancers.
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