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Gallic Acid Induces Apoptosis in Oral Squamous Cell Carcinoma via PI3K/AKT/mTOR Pathway Inhibition and PTEN

Sanaz Helli1, Armin Heidari1, Armin Tafvizi1

  • 1Department of Oral Medicine, TaMS.C., Islamic Azad University, Tabriz, Iran (the Islamic Republic of).

Drug Research
|November 26, 2025
PubMed

Insights

Gallic acid effectively reduced oral cancer cell viability by inhibiting the PI3K/AKT/mTOR pathway. This natural compound also activated apoptosis, showing promise for oral cancer targeted therapy.

Area of Science:

  • Oncology
  • Molecular Biology
  • Natural Product Chemistry

Background:

  • Oral squamous cell carcinoma (OSCC) presents significant challenges due to drug resistance and high mortality.
  • The Phosphatidylinositol 3-kinase/Protein kinase B/Mammalian target of rapamycin (PI3K/AKT/mTOR) pathway is critical for cancer cell survival, growth, and metastasis.
  • Targeting the PI3K/AKT/mTOR pathway offers a promising strategy for OSCC treatment.

Purpose of the Study:

  • To investigate the antitumor effects of gallic acid on OSCC CAL-27 cells.
  • To elucidate the impact of gallic acid on the PI3K/AKT/mTOR signaling pathway.
  • To assess the induction of apoptosis by gallic acid in OSCC cells.

Main Methods:

  • CAL-27 cells were treated with varying concentrations of gallic acid.
  • Cell viability was assessed using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay.
  • Gene and protein expression (PI3K/AKT/mTOR pathway, apoptosis markers) were analyzed via quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR) and Western blot.
  • Caspase-3/7 activity and apoptosis levels were quantified using fluorometric and enzyme-linked immunosorbent assay (ELISA) methods.

Main Results:

  • Gallic acid demonstrated a dose- and time-dependent reduction in OSCC cell viability.
  • Gallic acid treatment led to decreased expression of PI3K, AKT, and mTOR, and increased PTEN expression.
  • Upregulation of Bax expression and enhanced caspase activity confirmed gallic acid-induced apoptosis.

Conclusions:

  • Gallic acid exhibits potent anticancer properties against OSCC cells.
  • Inhibition of the PI3K/AKT/mTOR pathway and activation of apoptotic pathways are key mechanisms of gallic acid's action.
  • Gallic acid holds potential as a therapeutic agent for oral cancer, warranting further preclinical investigation.

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