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Updated: Oct 26, 2025

In Vitro and In Vivo Models to Study Corneal Endothelial-mesenchymal Transition
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Published on: August 20, 2016

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Vorinostat targets UBE2C to reverse epithelial-mesenchymal transition and control cervical cancer growth through the

Botao Pan1, Shuanghong Yin2, Fang Peng3

  • 1Foshan Maternal and Child Health Research Institute, South Medical University Affiliated Maternal & Child Health Hospital of Foshan, Foshan, 528000, China.

European Journal of Pharmacology
|July 31, 2021
PubMed

Insights

Vorinostat, a histone deacetylase inhibitor (HDACi), targets UBE2C to inhibit cervical cancer cell proliferation and reverse epithelial-mesenchymal transition. This study identifies UBE2C as a promising therapeutic target for cervical cancer treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Vorinostat (HDACi) previously inhibited cervical cancer cell proliferation, migration, and invasion via the PI3K/Akt pathway.
  • The precise molecular mechanisms of vorinostat in cervical cancer require further elucidation.
  • Identifying novel therapeutic targets is crucial for advancing cervical cancer treatment strategies.

Purpose of the Study:

  • To elucidate the molecular mechanism of vorinostat in cervical cancer treatment.
  • To identify potential molecular targets of vorinostat in cervical cancer.
  • To investigate the antitumor effect of vorinostat in vivo and in vitro.

Main Methods:

  • Utilized iTRAQ-based proteomics to identify differentially expressed proteins in vorinostat-treated cervical cancer cells.
  • Employed parallel reaction monitoring (PRM) technology for validation of proteomic findings.
  • Established a nude mouse xenograft model to assess in vivo antitumor efficacy.

Main Results:

  • Identified 254 differentially expressed proteins (180 upregulated, 74 downregulated) in vorinostat-treated cells.
  • UBE2C was identified as a promising target, with significantly higher expression in cancer cells than normal cells.
  • Vorinostat downregulated UBE2C, SQSTM1/p62, N-cadherin, vimentin, and upregulated E-cadherin, reversing epithelial-mesenchymal transition.

Conclusions:

  • Vorinostat reverses epithelial-mesenchymal transition in cervical cancer by targeting UBE2C.
  • Vorinostat controls cervical cancer cell proliferation through the ubiquitination pathway involving UBE2C.
  • UBE2C represents a promising therapeutic target for developing vorinostat-based cervical cancer treatment strategies.
Keywords:
Cervical cancerEpithelial-mesenchymal transitionUBE2CUbiquitinationVorinostatiTRAQ-based proteomics

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