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USP5 promotes glycolysis in cervical cancer by stabilizing FOXM1

Lili Su1, Ran Chen1, Tingting He1

  • 1Institute of Life Sciences, Youjiang Medical University for Nationalities Baise 533000, Guangxi Zhuang Autonomous Region, China.

American Journal of Cancer Research
|July 17, 2026
PubMed

Insights

Ubiquitin-specific peptidase 5 (USP5) drives cervical cancer by boosting cell growth and glycolysis while inhibiting cell death. Targeting USP5 offers a promising therapeutic strategy for cervical cancer management.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Cervical cancer treatment is hampered by limited efficacy, side effects, and high costs.
  • Identifying novel therapeutic targets is crucial for effective cervical cancer management.
  • The role of Ubiquitin-specific peptidase 5 (USP5) in cervical cancer remains unclear.

Purpose of the Study:

  • To investigate the role of USP5 in cervical cancer progression.
  • To explore the underlying mechanisms of USP5's function in cervical cancer.
  • To evaluate USP5 as a potential therapeutic target for cervical cancer.

Main Methods:

  • Bioinformatic and experimental assessment of USP5 expression.
  • Gain and loss of function studies in cervical cancer cell lines (Hela, CaSki) and a xenograft mouse model.
  • Quantitative polymerase chain reaction (RT-qPCR), cell counting kit-8 (CCK-8), clonogenesis, flow cytometry, western blot, co-immunoprecipitation (Co-IP), and immunohistochemistry assays were performed.

Main Results:

  • High USP5 expression correlated with poor prognosis in cervical cancer patients.
  • USP5 knockdown inhibited cell proliferation, glycolysis, and induced apoptosis.
  • USP5 overexpression promoted proliferation and glycolysis while suppressing apoptosis.
  • USP5 stabilized FOXM1 via deubiquitination, mediating its oncogenic effects.
  • USP5 silencing suppressed tumor growth and glycolytic gene expression in vivo.

Conclusions:

  • USP5 promotes cervical cancer progression by enhancing proliferation and glycolysis and suppressing apoptosis.
  • USP5 stabilizes FOXM1, which is critical for its oncogenic functions.
  • USP5 represents a potential therapeutic target for cervical cancer.
Keywords:
Cervical cancerFOXM1USP5deubiquitinationglycolysis

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