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Integration of Bioinformatics Approaches and Experimental Validations to Understand the Role of Notch Signaling in Ovarian Cancer
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Published on: January 12, 2020

Inhibition of the EP300/Notch Signaling Pathway Regulates Proliferation and Apoptosis in Oral Squamous Cell Carcinoma

Honglan Wang1,2,3, Yanzhen Fu1,2, Gaoren Lin4

  • 1Department of Stomatology, Affiliated Hospital of North Sichuan Medical College, Nanchong, China.

Journal of Oral Pathology & Medicine : Official Publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology
|June 16, 2026
PubMed
Abstract

Insights

EP300 drives oral squamous cell carcinoma (OSCC) growth by activating Notch signaling. Suppressing EP300 inhibits OSCC progression, offering a potential therapeutic target for this aggressive cancer.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Oral squamous cell carcinoma (OSCC) is characterized by high recurrence and metastasis rates.
  • The precise mechanisms by which EP300 contributes to OSCC tumorigenesis remain incompletely understood.
  • EP300 is implicated in various cellular processes relevant to cancer development.

Purpose of the Study:

  • To investigate the role of EP300 in OSCC.
  • To elucidate the mechanism underlying EP300-driven tumorigenesis in OSCC, focusing on its interplay with the Notch signaling pathway.
  • To assess the therapeutic potential of targeting EP300 in OSCC.

Main Methods:

  • EP300 expression analysis in OSCC cell lines and patient data using RT-PCR, Western blot, and bioinformatics.
  • Functional assays including CCK-8, colony formation, cell cycle, and apoptosis analysis following EP300 knockdown.
  • Investigation of EP300-Notch pathway interaction using Valproic acid (VPA) as a Notch signaling activator for rescue experiments.

Main Results:

  • EP300 was found to be significantly upregulated in OSCC cell lines and associated with poor patient prognosis.
  • EP300 knockdown suppressed OSCC cell proliferation, altered cell cycle progression, induced apoptosis, and inhibited epithelial-mesenchymal transition (EMT).
  • EP300 knockdown suppressed the Notch signaling pathway, and VPA treatment partially reversed the inhibitory effects of EP300 knockdown on OSCC cells.

Conclusions:

  • EP300 knockdown inhibits OSCC cell proliferation, cell cycle progression, and EMT while promoting apoptosis by suppressing the Notch signaling pathway.
  • EP300 plays a critical role in the growth and development of OSCC.
  • Targeting EP300 represents a promising therapeutic strategy for managing OSCC.
Keywords:
E1A‐binding protein p300apoptosisnotch signaling pathwayoral squamous cell carcinomaproliferation

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