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USP26 Promotes Cell Proliferation of Gastric Cancer by Stabilizing c-Myc.
Doudou Ren1,2, Zeqiong Cai2, Ru Zhang2
1Department of Gastroenterology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
DNA and Cell Biology
|October 22, 2025
Summary
Ubiquitin-specific peptidase 26 (USP26) promotes gastric cancer by stabilizing c-Myc, driving tumor growth and metabolism. Targeting USP26 offers a potential new therapeutic strategy for gastric cancer patients.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Gastric cancer is a leading cause of cancer mortality globally.
- Molecular mechanisms of gastric cancer progression are not fully understood.
- Deubiquitinases are emerging therapeutic targets, but a specific target for gastric cancer remains unidentified.
Purpose of the Study:
- To identify a novel deubiquitinase target for gastric cancer treatment.
- To investigate the role of ubiquitin-specific peptidase 26 (USP26) in gastric cancer progression.
Main Methods:
- Bioinformatics analysis to identify USP26.
- Short hairpin RNA (shRNA) to deplete USP26 in gastric cancer cells.
- Western blotting and co-immunoprecipitation to assess USP26-c-Myc interaction and protein stability.
Main Results:
- Upregulation of USP26 correlates with poor patient survival in gastric cancer.
- USP26 depletion suppresses aerobic glycolysis and proliferation of gastric cancer cells.
- USP26 interacts with and stabilizes c-Myc by inhibiting its polyubiquitination and degradation.
Conclusions:
- USP26 plays a novel oncogenic role in gastric cancer through a USP26-c-Myc regulatory axis.
- USP26 stabilizes the key oncoprotein c-Myc, promoting tumor metabolism and carcinogenesis.
- Targeting USP26 represents a potential therapeutic strategy for gastric cancer.
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