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[Allicin induced cell cycle arrest in human gastric cancer cell lines]

Min-wen Ha1, Yuan Yuan

  • 1Cancer Institute, First Affiliated Hospital of China Medical University, Shenyang 110001, China.

Zhonghua Zhong Liu Za Zhi [Chinese Journal of Oncology]
|January 7, 2005
PubMed
Abstract

Insights

Allicin halts the cell cycle in human gastric cancer cells at the M phase. This effect is linked to increased expression of p21WAF1 and p16INK4 genes, offering potential therapeutic insights.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Gastric cancer remains a significant global health challenge.
  • Allicin, a compound found in garlic, has demonstrated anti-cancer properties.
  • Understanding allicin's mechanism of action in gastric cancer is crucial for therapeutic development.

Purpose of the Study:

  • To investigate the impact of allicin on the cell cycle progression of human gastric cancer cell lines (MGC-803 and SGC-7901).
  • To elucidate the molecular mechanisms underlying allicin's effects on gastric cancer cells, focusing on cell cycle regulation and gene expression.

Main Methods:

  • Human gastric cancer cell lines (MGC-803 and SGC-7901) were treated with varying concentrations of allicin.
  • Cell proliferation was assessed using trypan-blue exclusion.
  • Morphological changes were examined via electron microscopy.
  • Cell cycle distribution was analyzed using flow cytometry and Giemsa staining.
  • The expression of p21WAF1 and p16INK4 (protein and mRNA) was quantified using immunohistochemistry and RT-PCR.

Main Results:

  • Allicin inhibited gastric cancer cell proliferation with IC50 values of 6.4 µg/ml (MGC-803) and 7.3 µg/ml (SGC-7901) after 24-hour exposure.
  • Higher allicin concentrations (≥ 12 µg/ml) induced cytotoxic effects, including membrane damage.
  • Allicin treatment (3-9 µg/ml for 24 hours) led to a significant decrease in G0/G1 phase cells and a significant increase in G2/M phase cells (P < 0.01).
  • Allicin (6 µg/ml for 24 hours) significantly increased the cell division index, indicating M phase arrest.
  • Expression of p21WAF1 and p16INK4 (protein and mRNA) was markedly upregulated in MGC-803 cells, and p21WAF1 in SGC-7901 cells.

Conclusions:

  • Allicin effectively induces cell cycle arrest in the M phase of human gastric cancer cells.
  • The observed M phase arrest is potentially mediated by the upregulation of p21WAF1 and p16INK4 gene expression.
  • These findings suggest allicin as a potential therapeutic agent for gastric cancer, warranting further investigation.

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