曲古抑菌素A对胃癌BGC823细胞增殖及凋亡的影响
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摘要
目的:研究曲古抑菌素A(TSA)对体外培养的胃癌BGC823细胞增殖及凋亡的影响。方法:体外培养人胃癌BGC823细胞,采用CCK8法测定不同浓度(100 nmol/L,200 nmol/L,300 nmol/L,400 nmol/L)及不同时间点(12 h、24 h、48 h)TSA对细胞增殖的影响。用流式细胞术检测48 h不同TSA浓度BGC823细胞的凋亡率。结果:CCK8法检测结果发现TSA对胃癌BGC823细胞有明显的增殖抑制作用,且呈浓度依赖性和时间依赖性。流式细胞术检测结果发现TSA可诱导人胃癌BGC823细胞凋亡,且呈浓度依赖性。结论:TSA可抑制体外培养的胃癌BGC823细胞生长,并可诱导其发生凋亡。
Objective:To study the effect of trichostatin A(TSA) on the proliferation and apoptosis of gastric cancer BGC823 cells in vitro.Methods:The proliferation of human gastric cancer BGC823 cells was detected by CCK8 method at different concentrations(100 nmol/L,200 nmol/L,300 nmol/L,400 nmol/L) and at different time points(12 h,24 h,48 h) Apoptosis rate of BGC823 cells treated with different TSA at 48 h was determined by cell cycle.Results:CCK8 assay showed that TSA had a significant inhibitory effect on gastric cancer BGC823 cells in a concentration-dependent and time-dependent manner.Flow cytometry showed that TSA could induce the apoptosis of human gastric cancer BGC823 cells in a concentration-dependent manner.Conclusion:TSA can inhibit the growth of gastric cancer BGC823 cells in vitro and induce apoptosis.
Objective:To study the effect of trichostatin A(TSA) on the proliferation and apoptosis of gastric cancer BGC823 cells in vitro.Methods:The proliferation of human gastric cancer BGC823 cells was detected by CCK8 method at different concentrations(100 nmol/L,200 nmol/L,300 nmol/L,400 nmol/L) and at different time points(12 h,24 h,48 h) Apoptosis rate of BGC823 cells treated with different TSA at 48 h was determined by cell cycle.Results:CCK8 assay showed that TSA had a significant inhibitory effect on gastric cancer BGC823 cells in a concentration-dependent and time-dependent manner.Flow cytometry showed that TSA could induce the apoptosis of human gastric cancer BGC823 cells in a concentration-dependent manner.Conclusion:TSA can inhibit the growth of gastric cancer BGC823 cells in vitro and induce apoptosis.
引文
[1]LI Y L,YANG T S,RUAN W M,et al.Effect of trichostatin a on SGC-7901 gastric cancer cells[J].Int J Clin Exp Med,2014,7(8):1958-1966.
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[5]BAJBOUJ K,MAWRIN C,HARTIG R,et al.P53-dependent antiproliferative and pro-apoptotic effects of trichostatin A (TSA) in glioblastoma cells[J].J Neurooncol,2012,107(3):503-516.
[6]BUTLER LM,WEBB Y,AGUS D B,et al.Inhibition of transformed cell growth and induction of cellular differentiation by pyroxamide,an inhibitor of histone deacetylase[J].Clin Cancer Res,2001,7(4):962-970.
[7]PAUL A M.The clinical development of histone deacetylase inhibitors as targeted anticancer drugs[J].Expert opininvestig drugs,2010,19(9):1049-1066.
[8]LAKSHMAIAH K C,JACOB L A,APARNA S,et al.Ep-igenetic therapy of cancer with histone deacetylase inhibitors[J].J Cancer Res Ther,2014,10(3):469-478.
[9]NIEGISCH G,KNIEVEL J,KOCH A,et al.Changes in histone deacetylase (HDAC) expression patterns and activity of HDAC inhibitors in urothelial cancers[J].Urol Oncol,2013,31(8):1770-1779.
[10]HENKENS T,PAPELEU P,ELAUT G,et al.Trichostatin A,a critical factor in main taining the functional differentiation of primary cultured rat hepatocytes[J].Toxicol Appl Pharmacol,2007,218(1):64-71.
[11]CHIBA T,YOKOSUKA O,FUKAI K,et al.Cell growth inhibition and gene expression induced by the histone deacetylase inhibitor,trichostatin A,on human hepatoma cells[J].Onclogy,2004,66(6):481-491.
[12]CHEN C Q,CHEN C S,CHEN J J,et al.Histone deacetylases inhibitor trichostatin A increases the expression of Dleu2/miR-15a/16-1 via HDAC3 in non-small cell lung cancer[J].Mol Cel Biochem,2013,383(1-2):137-148.
[2]SHANKAR S,SRIVASTAVA R K.Histone deacetylase inhibitors:mechanisms and clinical significance in cancer:HDAC inhibitor-induced apoptosis[J].Adv Exp Med Biol,2008,615:261-298.
[3]CHIBA T,YOKOSUKA O,FUKAI K,et al.Cell growth inhibition and gene expression induced by the histone deacetylase inhibitor,trichostatin A,on human hepatoma cells[J].Oncology,2004,66(6):481-491.
[4]CHEN C Q,CHEN C S,CHEN J J,et al.Histone deacetylases inhibitor trichostatin A increases the expression of Dleu2/miR-15a/16-1 via HDAC3 in non-small cell lung cancer[J].Molecular and cellular biochemistry,2013,383(1-2):137-148.
[5]BAJBOUJ K,MAWRIN C,HARTIG R,et al.P53-dependent antiproliferative and pro-apoptotic effects of trichostatin A (TSA) in glioblastoma cells[J].J Neurooncol,2012,107(3):503-516.
[6]BUTLER LM,WEBB Y,AGUS D B,et al.Inhibition of transformed cell growth and induction of cellular differentiation by pyroxamide,an inhibitor of histone deacetylase[J].Clin Cancer Res,2001,7(4):962-970.
[7]PAUL A M.The clinical development of histone deacetylase inhibitors as targeted anticancer drugs[J].Expert opininvestig drugs,2010,19(9):1049-1066.
[8]LAKSHMAIAH K C,JACOB L A,APARNA S,et al.Ep-igenetic therapy of cancer with histone deacetylase inhibitors[J].J Cancer Res Ther,2014,10(3):469-478.
[9]NIEGISCH G,KNIEVEL J,KOCH A,et al.Changes in histone deacetylase (HDAC) expression patterns and activity of HDAC inhibitors in urothelial cancers[J].Urol Oncol,2013,31(8):1770-1779.
[10]HENKENS T,PAPELEU P,ELAUT G,et al.Trichostatin A,a critical factor in main taining the functional differentiation of primary cultured rat hepatocytes[J].Toxicol Appl Pharmacol,2007,218(1):64-71.
[11]CHIBA T,YOKOSUKA O,FUKAI K,et al.Cell growth inhibition and gene expression induced by the histone deacetylase inhibitor,trichostatin A,on human hepatoma cells[J].Onclogy,2004,66(6):481-491.
[12]CHEN C Q,CHEN C S,CHEN J J,et al.Histone deacetylases inhibitor trichostatin A increases the expression of Dleu2/miR-15a/16-1 via HDAC3 in non-small cell lung cancer[J].Mol Cel Biochem,2013,383(1-2):137-148.