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USP7 Stabilizes MESP1 To Promote the Malignant Progression of Non-Small Cell Lung Cancer
Shasha Jiang1, Liwen Rong2, Fei Yi3
1Department of Oncology, The Third People's Hospital of Chengdu, No.82 Qinglong Street, Qingyang District 610031, Chengdu, Sichuan, China. 15902891862@163.com.
Applied Biochemistry and Biotechnology
|January 21, 2026
Summary
Mesoderm posterior bHLH transcription factor 1 (MESP1) and ubiquitin specific peptidase 7 (USP7) are upregulated in non-small cell lung cancer (NSCLC). Targeting the USP7-MESP1 axis inhibits NSCLC progression by stabilizing MESP1, offering a potential new therapy.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Non-small cell lung cancer (NSCLC) is a major cause of cancer mortality globally.
- Novel therapeutic targets for NSCLC are urgently needed.
- The role of Mesoderm posterior bHLH transcription factor 1 (MESP1) in NSCLC is not well understood.
Purpose of the Study:
- To investigate the role of MESP1 and its regulatory mechanisms in NSCLC.
- To explore the potential of targeting the MESP1 pathway for NSCLC therapy.
Main Methods:
- Quantitative real-time PCR (qRT-PCR) and Western blotting to assess MESP1 and USP7 expression.
- Cellular assays (proliferation, apoptosis, ferroptosis markers) and in vivo xenograft models to evaluate MESP1 function.
- Co-immunoprecipitation and ubiquitination assays to elucidate the interaction between USP7 and MESP1.
Main Results:
- MESP1 and USP7 were upregulated in NSCLC tissues and cells.
- MESP1 knockdown inhibited proliferation, induced apoptosis and ferroptosis, and suppressed tumor formation in NSCLC.
- USP7 deubiquitinates and stabilizes MESP1, promoting NSCLC progression.
Conclusions:
- USP7 stabilizes MESP1, contributing to the malignant progression of NSCLC.
- The USP7-MESP1 axis represents a promising therapeutic target for NSCLC treatment.
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