Apigenin impairs oral squamous cell carcinoma growth in vitro inducing cell cycle arrest and apoptosis

Daniele Maggioni1, Werner Garavello, Roberta Rigolio

  • 1Department of Surgery and Translational Medicine, University of Milan-Bicocca, I-20900 Monza, Italy.

Insights

Apigenin, a plant flavonoid, shows anticancer potential against oral cancer cells (SCC-25) by reducing growth and inducing apoptosis. It effectively modulates the cell cycle, suggesting promise as a chemopreventive agent.

Area of Science:

  • Phytochemistry
  • Molecular Biology
  • Cancer Research

Background:

  • Flavonoids, like apigenin found in fruits and vegetables, are studied for their health benefits.
  • Oral squamous cell carcinoma (OSCC) is a significant global health concern requiring novel therapeutic strategies.

Purpose of the Study:

  • To investigate the antiproliferative mechanisms of apigenin in an oral cancer cell line (SCC-25) and a keratinocyte cell line (HaCaT).
  • To evaluate apigenin's potential as an anticancer and chemopreventive agent.

Main Methods:

  • Cell viability assessed using MTT assay.
  • Apoptosis evaluated via phosphatidyl serine membrane translocation.
  • Cell cycle distribution analyzed by flow cytometry using propidium iodide staining.
  • Expression of cyclins and cyclin-dependent kinases (CDKs) determined by western blotting.

Main Results:

  • Apigenin reduced cell growth in both SCC-25 and HaCaT cells, with SCC-25 cells showing higher sensitivity.
  • Apigenin induced apoptosis and modulated the cell cycle in SCC-25 cells.
  • Cell cycle arrest occurred at G0/G1 and G2/M checkpoints, with decreased cyclin D1/E expression and CDK1 inactivation.

Conclusions:

  • Apigenin exhibits significant anticancer potential against oral squamous cell carcinoma cells.
  • Apigenin acts as a cell cycle modulating agent at multiple levels, supporting its role as a chemopreventive agent.
  • Further research into apigenin's therapeutic applications in oral cancer is warranted.

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