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目的研究组蛋白去乙酰化酶(HDACs)抑制剂西达本胺对胃癌细胞株体外抗增殖作用及其可能机制。方法用西达本胺终浓度为0、16、32、64、128、256μmol/L(分别为B、A1、A2、A3、A4、A5组)处理SGC-7901细胞24、48、72h。采用MTT法及流式细胞术分别检测细胞增殖及细胞凋亡,反转录PCR(RT-PCR)检测沉默信息调节因子2相关酶1(SIRT1)及HDAC11mRNA表达,实时荧光定量PCR(RT-qPCR)检测表皮生长因子受体(EGFR)mRNA表达,Western blot检测Notch1蛋白的表达。结果与B组相比,西达本胺呈浓度依赖性地抑制SGC-7901细胞增殖(P<0.05),提高SGC-7901细胞凋亡率(P<0.05),阻断SIRT1、HDAC11、EGFR mRNA以及Notch1蛋白表达(P<0.05)。结论西达本胺可抑制SGC-7901细胞增殖,促进细胞凋亡;其作用机制可能是降低SIRT1、HDAC11基因的表达或与Notch及EGFR信号通路相关。
Objective To study the anti-proliferation effect of histamine deacetylase (HDACs) inhibitor cedostine on gastric cancer cell lines in vitro and its possible mechanism. Methods SGC-7901 cells were treated with 0, 16, 32, 64, 128 and 256 μmol / L of cedostine for 24, 48, and 72 hours respectively (groups B, A1, A2, A3, A4 and A5). Cell proliferation and apoptosis were detected by MTT assay and flow cytometry respectively. The expression of SIRT1 and HDAC11 mRNA was detected by reverse transcription-polymerase chain reaction (RT-PCR). Real-time PCR (RT-qPCR ) To detect the expression of epidermal growth factor receptor (EGFR) mRNA, Western blot detection of Notch1 protein expression. Results Compared with group B, cistamine inhibited the proliferation of SGC-7901 cells in a dose-dependent manner (P <0.05), and increased the apoptosis rate of SGC-7901 cells (P <0.05) and blocked the expression of SIRT1, HDAC11 and EGFR mRNA And Notchl protein expression (P <0.05). CONCLUSION: Cedilamine can inhibit the proliferation and promote the apoptosis of SGC-7901 cells. Its mechanism may be to reduce the expression of SIRT1 and HDAC11 genes or to be involved in Notch and EGFR signaling pathways.