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Updated: Jun 4, 2025

In Vitro Ubiquitination and Deubiquitination Assays of Nucleosomal Histones
Published on: July 25, 2019
USP37 promotes diffuse large B-cell lymphoma progression by deubiquitinating and stabilizing c-myc
Ying Li1, Wei Wang1, Lingjie Sun1
1Department of Hematology, The Affiliated Hospital of Qingdao University, Qingdao University, No. 16 Jiangsu Road, Qingdao, 266000, Shandong Province, China.
Ubiquitin-specific peptidase 37 (USP37) promotes diffuse large B cell lymphoma (DLBCL) growth by stabilizing c-myc. USP37 inhibition hinders DLBCL progression, suggesting it as a potential therapeutic target for this lymphoma subtype.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Diffuse large B cell lymphoma (DLBCL) with MYC and BCL2 co-expression (
- double expressor lymphomas
- ) has a poorer prognosis.
- The role of ubiquitin-specific peptidase 37 (USP37) in stabilizing c-myc is known in lung cancer but unexplored in DLBCL.
Purpose of the Study:
- To investigate the role and mechanism of USP37 in DLBCL pathogenesis.
- To evaluate USP37 as a potential therapeutic target for DLBCL.
Main Methods:
- Detection of USP37 expression in DLBCL tissues and cells using RT-PCR, immunohistochemistry, and Western blot.
- In vitro studies involving transfection of DLBCL cells with si-USP37.
- In vivo studies using mouse xenograft models.
Main Results:
- USP37 expression was elevated in DLBCL tissues and cells.
- USP37 knockdown in DLBCL cells reduced proliferation and promoted cell cycle arrest.
- USP37 deubiquitinates and stabilizes c-myc, promoting DLBCL cell proliferation and cell cycle progression.
- USP37 depletion inhibited tumor xenograft development in mice, an effect partially reversed by c-myc overexpression.
Conclusions:
- USP37 promotes DLBCL progression by stabilizing c-myc.
- USP37 is a potential therapeutic target for DLBCL, particularly for "double expressor lymphomas".
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