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Artemisinin: an alternative treatment for oral squamous cell carcinoma

Eiki Yamachika1, Temesgen Habte, Dolphine Oda

  • 1Department of Oral and Maxillofacial Surgery, School of Dentistry, University of Washington, Box 357134, Seattle, WA 98195-7134, USA.

Anticancer Research
|August 28, 2004
PubMed

Insights

Artemisinin (AR) induces apoptosis in transformed oral epithelial cells, showing significant cytotoxicity. In contrast, 5-fluorouracil (5-FU) primarily causes cell toxicity with less apoptosis.

Area of Science:

  • Oncology
  • Pharmacology
  • Cell Biology

Background:

  • Artemisinin (AR), a known antimalarial, exhibits emerging anticancer properties.
  • Human gingival epithelial (IHGK) cells, immortalized and transformed by HPV 16, serve as a model for oral cancer research.

Purpose of the Study:

  • To investigate the cytotoxic effects of Artemisinin (AR) and 5-fluorouracil (5-FU) on HPV 16-transformed human gingival epithelial (IHGK) cells.
  • To elucidate the mechanisms of cell death induced by AR and 5-FU in these cells.

Main Methods:

  • Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay to detect apoptosis.
  • Immunohistochemistry (IHS) for apoptosis-related markers (Bax, p53, Bcl-2) and co-stimulatory molecules (CD40, CD40L).
  • Flow cytometry to analyze cell cycle progression.

Main Results:

  • TUNEL assay revealed 82% apoptosis in AR-treated IHGK cells versus 18% in 5-FU-treated cells.
  • AR treatment upregulated pro-apoptotic markers (Bax, p53) and co-stimulatory molecules (CD40, CD40L) while downregulating anti-apoptotic Bcl-2.
  • 5-FU induced similar but less intense marker changes and a significant increase in S-phase (45%), indicating cell cycle arrest.

Conclusions:

  • Artemisinin (AR) demonstrates potent cytotoxicity against transformed oral epithelial cells, primarily through the induction of apoptosis.
  • 5-fluorouracil (5-FU) exhibits cytotoxicity mainly via non-apoptotic cell toxicity mechanisms, including S-phase arrest.