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目的研究抑制组蛋白去乙酰化酶1(HDAC1)后对人胃癌干细胞(GCSGs)增殖、干性及侵袭作用的影响。方法以CD44为胃癌干性标志物,流式分选出GCSCs。实时荧光定量核酸扩增检测(RT-qPCR)和蛋白免疫印迹法(Western blot)分别检测GCSGs与胃癌非干细胞中HDAC1的表达量。组蛋白去乙酰化酶抑制剂处理GCSCs后,CCK-8法、克隆形成和Transwell实验观察细胞增殖和侵袭的变化;RT-qPCR和Western blot检测其对凋亡、侵袭相关蛋白及干性标志物表达的影响。结果 HDAC1在GCSCs中的表达比胃癌非干细胞高。实验组细胞的增殖和侵袭能力相较于对照组均减弱,且下调干性标志物及介导上皮间质转化。结论抑制HDAC1的去乙酰化作用后GCSCs的增殖、干性及侵袭能力降低。
Objective To investigate the effects of inhibiting histone deacetylase 1 (HDAC1) on the proliferation, stemness and invasion of human gastric cancer stem cells (GCSGs). Methods CD44 was used as a marker of gastric cancer and GCSCs were separated by flow cytometry. Real-time fluorescence quantitative PCR (RT-qPCR) and Western blot were used to detect the expression of HDAC1 in GCSGs and gastric cancer non-stem cells respectively. After treatment of GCSCs with histone deacetylase inhibitors, the changes of cell proliferation and invasion were observed by CCK-8 assay, clone formation and Transwell assay. The expressions of apoptosis-related proteins, invasion-related proteins and dry markers were detected by RT-qPCR and Western blot The impact of expression. Results The expression of HDAC1 in GCSCs was higher than that of non-stem cells in gastric cancer. Compared with the control group, the proliferation and invasion ability of the experimental group cells were weakened, and down-regulated the dry markers and mediated the epithelial-mesenchymal transition. Conclusion Inhibition of HDAC1 deacetylation GCSCs proliferation, dry and invasive ability decreased.