Knockdown of TFAP2E results in rapid G2/M transition in oral squamous cell carcinoma cells

Ryo Sakai1,2, Kyoko Fujiwara3,4, Eri Nagasaki-Maeoka5

  • 1Department of Periodontology, Nihon University School of Dentistry, Tokyo 101-8310, Japan.

Oncology Letters
|February 9, 2024
PubMed

Insights

Transcription factor AP-2E (TFAP2E) downregulation accelerates oral squamous cell carcinoma (OSCC) proliferation. TFAP2E may suppress OSCC by regulating the G2/M cell cycle transition.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Transcription factor AP-2E (TFAP2E) functions as a tumor suppressor in various cancers.
  • Reduced TFAP2E expression correlates with poorer survival in oral squamous cell carcinoma (OSCC) patients.

Purpose of the Study:

  • To elucidate the molecular mechanisms underlying TFAP2E's tumor-suppressive role in OSCC.
  • To investigate the impact of TFAP2E downregulation on OSCC cell proliferation and cell cycle progression.

Main Methods:

  • Utilized small interfering RNA (siRNA) to knockdown TFAP2E expression in OSCC cell lines (Ca9-22, HSC-4).
  • Assessed cell proliferation using the water-soluble tetrazolium salt-8 (WST-8) assay.
  • Analyzed cell cycle distribution and M phase entry using fluorescence-activated cell sorting (FACS) and histone H3 Serine 28 phosphorylation marker.

Main Results:

  • TFAP2E knockdown significantly increased OSCC cell proliferation compared to controls.
  • While overall cell cycle profiles showed no major differences, TFAP2E-knockdown cells exhibited a higher rate of entry into M phase, indicated by increased histone H3 Serine 28 phosphorylation.
  • These findings suggest a role for TFAP2E in regulating the G2/M cell cycle transition.

Conclusions:

  • TFAP2E downregulation promotes OSCC cell proliferation.
  • TFAP2E appears to attenuate OSCC progression by modulating the G2/M phase transition, highlighting its potential as a therapeutic target.

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