OBJECTIVE: To determine the effect of beta-ionone on the potential metastasis of human gastric adenocarcinoma cell line SGC-7901 and the underlying mechanism. METHODS: Using curve of cellular growth, Zymograms, and RT-PCR assays, we analyzed the growth rate, the activities of two types IV collagenase of Matrix met alloproteinase 9 (MMP-9) and MMP-2 and the expression of nm23-H1 gene, tissue inhibitor of met alloproteinase 1 (TIMP-1) and TIMP-2 in SGC-7901 cells which were treated with progressively increasing concentrations (25, 50, 100 and 200 micromol/L) of beta-ionone for 24 h and 48 h. RESULTS: The growth of SGC-7901 cells was inhibited by beta-ionone. Eight days after treatment with different concentrations of beta-ionone, as mentioned above, the inhibition rates were 25.93%, 28.21%, 74.36% and 90.11%, respectively compared to the negative control. The estimated IC50 value of beta-ionone for SGC-7901 cells was estimated to be 89 micromol/L; beta-ionone did not show any effect on the activities of MMP-9 and MMP-2 in SGC-7901 cells. However, the expression of nm23-H1, TIMP-1 and TIMP-2 mRNA transcripts gradually increased in response to beta-ionone in a dose-dependent manner. CONCLUSION: beta-ionone can inhibit the growth and proliferation of SGC-7901 cells. It may show some effects on the potential metastasis of SGC-7901 cells indicates by its upregulation of nm23-H1, TIMP-1 and TIMP-2 expression. However, beta-ionone may have no effect on the activities of type IV collagenase in SGC-7901 cells. The mechanism by which beta-ionone inhibits the potential metastasis of SGC-7901 cells needs to be studied further.
OBJECTIVE: To determine the effect of beta-ionone on the potential metastasis of humangastric adenocarcinoma cell line SGC-7901 and the underlying mechanism. METHODS: Using curve of cellular growth, Zymograms, and RT-PCR assays, we analyzed the growth rate, the activities of two types IV collagenase of Matrix met alloproteinase 9 (MMP-9) and MMP-2 and the expression of nm23-H1 gene, tissue inhibitor of met alloproteinase 1 (TIMP-1) and TIMP-2 in SGC-7901 cells which were treated with progressively increasing concentrations (25, 50, 100 and 200 micromol/L) of beta-ionone for 24 h and 48 h. RESULTS: The growth of SGC-7901 cells was inhibited by beta-ionone. Eight days after treatment with different concentrations of beta-ionone, as mentioned above, the inhibition rates were 25.93%, 28.21%, 74.36% and 90.11%, respectively compared to the negative control. The estimated IC50 value of beta-ionone for SGC-7901 cells was estimated to be 89 micromol/L; beta-ionone did not show any effect on the activities of MMP-9 and MMP-2 in SGC-7901 cells. However, the expression of nm23-H1, TIMP-1 and TIMP-2 mRNA transcripts gradually increased in response to beta-ionone in a dose-dependent manner. CONCLUSION:beta-ionone can inhibit the growth and proliferation of SGC-7901 cells. It may show some effects on the potential metastasis of SGC-7901 cells indicates by its upregulation of nm23-H1, TIMP-1 and TIMP-2 expression. However, beta-ionone may have no effect on the activities of type IV collagenase in SGC-7901 cells. The mechanism by which beta-ionone inhibits the potential metastasis of SGC-7901 cells needs to be studied further.