Chinese Clinical Oncology
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ZENG Fanye, FAN Yuxiang, ZHANG Hongliang.
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Abstract: Objective To explore the effects of β-carboline alkaloid on the proliferation, apoptosis and expression levels of phosphatase and tensin homologue deleted on chromosome 10(PTEN)/serine-threonine kinase(Akt) in human gastric cancer SGC-7901 cells. Methods SGC-7901 cells were treated with different concentrations of β-carboline alkaloid. Cell viability was measured by CCK-8 at 24 and 48 h after the treatment of β-carboline alkaloid(0, 10, 20, 40 μg/ml). Apoptosis morphological and biochemical changes were detected by Hoechst 33258 staining and agarose gel electroghoresis at 48 h after the treatment of β-carboline alkaloid, respectively. The mRNA and protein levels of PTEN and Akt were examined by quantitative reverse-transcription PCR and Western blotting at 48 h after the treatment of β-carboline alkaloid(0, 10, 20, 30, 40 μg/ml). Results β-carboline alkaloid effectively inhibited the proliferation of SGC-7901 cells in a concentration-dependent manner. β-carboline alkaloid could induce the apoptosis of SGC-7901 cells with the characteristic ladder pattern. Compared with 0 μg/ml, there were increased mRNA and protein levels of PTEN but decreased mRNA and protein levels of Akt in other concentrations of β-carboline alkaloid with significant difference(P<0.05). Conclusion β-carboline alkaloid inhibited the cell prolifetation and induced cell apoptosis, with the possible mechanism of up-regulation of anti-apoptotic protein PTEN and down-regulation of apoptotic protein Akt.
Objective To explore the effects of β-carboline alkaloid on the proliferation, apoptosis and expression levels of phosphatase and tensin homologue deleted on chromosome 10(PTEN)/serine-threonine kinase(Akt) in human gastric cancer SGC-7901 cells. Methods SGC-7901 cells were treated with different concentrations of β-carboline alkaloid. Cell viability was measured by CCK-8 at 24 and 48 h after the treatment of β-carboline alkaloid(0, 10, 20, 40 μg/ml). Apoptosis morphological and biochemical changes were detected by Hoechst 33258 staining and agarose gel electroghoresis at 48 h after the treatment of β-carboline alkaloid, respectively. The mRNA and protein levels of PTEN and Akt were examined by quantitative reverse-transcription PCR and Western blotting at 48 h after the treatment of β-carboline alkaloid(0, 10, 20, 30, 40 μg/ml). Results β-carboline alkaloid effectively inhibited the proliferation of SGC-7901 cells in a concentration-dependent manner. β-carboline alkaloid could induce the apoptosis of SGC-7901 cells with the characteristic ladder pattern. Compared with 0 μg/ml, there were increased mRNA and protein levels of PTEN but decreased mRNA and protein levels of Akt in other concentrations of β-carboline alkaloid with significant difference(P<0.05). Conclusion β-carboline alkaloid inhibited the cell prolifetation and induced cell apoptosis, with the possible mechanism of up-regulation of anti-apoptotic protein PTEN and down-regulation of apoptotic protein Akt.
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URL: http://manu65.magtech.com.cn/Jwk3_lczlxzz/EN/
http://manu65.magtech.com.cn/Jwk3_lczlxzz/EN/Y2016/V21/I2/126
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