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DPY30 regulates cervical squamous cell carcinoma by mediating epithelial-mesenchymal transition (EMT)

Feng-Xi He1, Li-Li Zhang1, Peng-Fei Jin1

  • 1Department of Obstetrics and Gynecology, Liaocheng People's Hospital Affiliated to Shandong First Medical University, Liaocheng 252000, People's Republic of China.

Oncotargets and Therapy
|October 1, 2019
PubMed
Abstract

Insights

Elevated DPY30 levels promote cervical squamous cell carcinoma (CSCC) progression by enhancing epithelial-mesenchymal transition (EMT) through Wnt/β-catenin signaling. Reducing DPY30 inhibits CSCC cell growth, migration, and invasion.

Area of Science:

  • Oncology
  • Molecular Biology
  • Epigenetics

Background:

  • Set1/MLL complexes are key histone H3K4 methyltransferases involved in tumor pathogenesis.
  • DPY30, a component of Set1/MLL, is implicated in tumor growth, but its role in cervical squamous cell carcinoma (CSCC) is unclear.

Purpose of the Study:

  • To investigate the molecular mechanisms of DPY30 in the progression of cervical squamous cell carcinoma (CSCC).

Main Methods:

  • Analyzed DPY30 expression in CSCC tissues using immunohistochemistry and real-time PCR.
  • Assessed DPY30 and epithelial-mesenchymal transition (EMT) markers in a human cervical cancer cell line in vitro.
  • Utilized siRNA to knock down DPY30 expression and evaluated its effects on CSCC cell behavior and signaling pathways.

Main Results:

  • DPY30 expression was significantly upregulated in CSCC tissues and correlated with EMT markers like E-cadherin.
  • DPY30 knockdown reduced CSCC cell proliferation, migration, and invasion.
  • DPY30-induced EMT was found to be mediated by the Wnt/β-catenin signaling pathway.

Conclusions:

  • Elevated DPY30 expression contributes to CSCC progression by promoting EMT.
  • Activation of Wnt/β-catenin signaling by DPY30 is a key mechanism in CSCC development.
Keywords:
DPY30Wnt/β-catenin pathwaycervical squamous cell carcinomaepithelial–mesenchymal transition

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