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USP3 Promotes Glioma Progression by Stabilizing PLK1 through Deubiquitination.

Feng Yan1,2,3, Yongzhi Shan1,2,3, Yaming Wang1,2,3

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|January 12, 2026
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USP3 deubiquitinating enzyme stabilizes PLK1, promoting glioma progression and malignancy. Targeting the USP3-PLK1 axis offers a potential therapeutic strategy for aggressive brain tumors.

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Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Glioma is an aggressive brain tumor demanding new therapeutic targets.
  • Ubiquitination and deubiquitination pathways are crucial in cancer progression.
  • USP3 (deubiquitinating enzyme) and PLK1 (cell cycle kinase) are implicated in cancer proliferation.

Purpose of the Study:

  • To investigate if USP3 modulates PLK1 via deubiquitination, influencing glioma progression.
  • To analyze USP3 expression in glioma tissues.
  • To determine the mechanistic link between USP3, PLK1, and glioma malignancy.

Main Methods:

  • TCGA datasets for USP3 expression analysis.
  • Gain-of-function (USP3 overexpression) and loss-of-function (USP3 knockdown) cell models.
  • Cell proliferation (CCK-8), cell cycle (flow cytometry), migration/invasion (Transwell) assays.
  • Nude mouse xenografts and PCNA immunohistochemistry.
  • Co-immunoprecipitation and Western blotting to assess protein interactions and ubiquitination.

Main Results:

  • USP3 was upregulated in glioma tissues.
  • USP3 overexpression increased glioma cell proliferation, cell cycle progression, and invasion.
  • USP3 knockdown suppressed these malignant phenotypes.
  • USP3 deubiquitinates and stabilizes PLK1 by reducing K48-linked ubiquitination.
  • USP3 knockdown increased PLK1 ubiquitination and decreased PLK1 abundance.
  • Tumor xenografts showed increased growth and PCNA levels with USP3 overexpression, and reduced growth with knockdown.

Conclusions:

  • USP3 promotes glioma malignancy by deubiquitinating and stabilizing PLK1.
  • This stabilization enhances glioma cell proliferation and invasion.
  • The USP3-PLK1 axis represents a potential therapeutic target for glioma treatment.