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Sapylin-induced apoptosis of SGC7901 gastric cancer cells and its mechanism

Feng Ming-xuan

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Abstract

Objective:To investigate the apoptosis of SGC7901 human gastric cancer cells induced by sapylin and its molecular mechanism. Methods: SGC7901 cells were treated with 0, 0.001, 0.01, 0.1 and 0.5 KE /ml sapylin for 6, 12, 24 and 48 hours respectively. The cell proliferation was detected by MTT assay, the cell apoptosis observed by flow cytometry with Annexin V and propidium iodide double staining, and the expressions of survivin mRNA and caspase-3 mRNA detected by semi-quantitive RT-PCR. Results: Sapylin effectively inhibited the proliferation of SGC7901 cells in a dose-and time-dependent manner. After 48 hours of sapylin treatment, the apoptosis of SGC7901 cells was increased in a dose-dependent manner. Compared with the control group, the expression of survivin mRNA was significantly decreased (P 0.05), while that of caspase-3 mRNA markedly upregulated in the sapylin group(P 0.05). Conclusion: Sapylin inhibits the proliferation and induces the apoptosis of SGC7901 cells, which suggests its potential value for the treatment of human gastric cancer. The molecular mechanism of sapylin inducing the apoptosis of SGC7901 gastric cancer cells may be associated with its action of up-regulating the expression of caspase-3 mRNA and down-regulating the expression of survivin mRNA.

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Objective:To investigate the apoptosis of SGC7901 human gastric cancer cells induced by sapylin and its molecular mechanism. Methods: SGC7901 cells were treated with 0, 0.001, 0.01, 0.1 and 0.5 KE /ml sapylin for 6, 12, 24 and 48 hours respectively. The cell proliferation was detected by MTT assay, the cell apoptosis observed by flow cytometry with Annexin V and propidium iodide double staining, and the expressions of survivin mRNA and caspase-3 mRNA detected by semi-quantitive RT-PCR. Results: Sapylin effectively inhibited the proliferation of SGC7901 cells in a dose-and time-dependent manner. After 48 hours of sapylin treatment, the apoptosis of SGC7901 cells was increased in a dose-dependent manner. Compared with the control group, the expression of survivin mRNA was significantly decreased (P 0.05), while that of caspase-3 mRNA markedly upregulated in the sapylin group(P 0.05). Conclusion: Sapylin inhibits the proliferation and induces the apoptosis of SGC7901 cells, which suggests its potential value for the treatment of human gastric cancer. The molecular mechanism of sapylin inducing the apoptosis of SGC7901 gastric cancer cells may be associated with its action of up-regulating the expression of caspase-3 mRNA and down-regulating the expression of survivin mRNA.

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Available abstract

Objective:To investigate the apoptosis of SGC7901 human gastric cancer cells induced by sapylin and its molecular mechanism. Methods: SGC7901 cells were treated with 0, 0.001, 0.01, 0.1 and 0.5 KE /ml sapylin for 6, 12, 24 and 48 hours respectively. The cell proliferation was detected by MTT assay, the cell apoptosis observed by flow cytometry with Annexin V and propidium iodide double staining, and the expressions of survivin mRNA and caspase-3 mRNA detected by semi-quantitive RT-PCR. Results: Sapylin effectively inhibited the proliferation of SGC7901 cells in a dose-and time-dependent manner. After 48 hours of sapylin treatment, the apoptosis of SGC7901 cells was increased in a dose-dependent manner. Compared with the control group, the expression of survivin mRNA was significantly decreased (P 0.05), while that of caspase-3 mRNA markedly upregulated in the sapylin group(P 0.05). Conclusion: Sapylin inhibits the proliferation and induces the apoptosis of SGC7901 cells, which suggests its potential value for the treatment of human gastric cancer. The molecular mechanism of sapylin inducing the apoptosis of SGC7901 gastric cancer cells may be associated with its action of up-regulating the expression of caspase-3 mRNA and down-regulating the expression of survivin mRNA.

Key concepts: Survivin, Apoptosis, Propidium iodide, Annexin, Flow cytometry, Cancer cell, Molecular biology, Messenger RNA

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