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作 者:焦韵苹[1] 张珩 李思维 宋宵 JIAO Yunping;ZHANG Heng;LI Siwei;SONG Xiao(Clinical Pharmacy Department,the Second People's Hospital of Shaanxi,Xi'an 710005;Pharmacy Department,Northwest Women's and Children's Hospital,Xi'an 710000,China)
机构地区:[1]陕西省第二人民医院临床药学部,陕西西安710005 [2]西北妇女儿童医院药剂科,陕西西安710000
出 处:《临床医学研究与实践》2020年第28期5-8,共4页Clinical Research and Practice
摘 要:目的探讨和厚朴酚对鼻咽癌细胞(HK1和CNE2细胞株)增殖、迁移和侵袭的分子机制。方法采用CCK-8试剂盒检测HK1和CNE2细胞的活性,集落形成试验检测HK1和CNE2细胞的生长情况,Caspase-3活性试剂盒检测HK1和CNE2细胞的Caspase-3活性。采用划痕愈合试验和Transwell侵袭试验分别检测HK1和CNE2细胞的迁移和侵袭能力,实时荧光定量PCR检测HK1和CNE2细胞中N-cadherin mRNA和vimentin mRNA的表达水平。结果采用浓度为20、40、80μM的和厚朴酚处理HK1和CNE2细胞24、48 h后,细胞的活性均低于对照组(P<0.05)。相较于对照组,40μM和厚朴酚可抑制HK1和CNE2细胞集落形成数量,提高细胞中Caspase-3的活性,降低HK1和CNE2细胞的划痕愈合率和侵袭数量,下调HK1和CNE2细胞中N-cadherin mRNA及vimentin mRNA的表达(P<0.05)。结论和厚朴酚能够通过促进凋亡和抑制上皮间质转换来抑制鼻咽癌细胞的增殖、迁移以及侵袭。Objective To investigate the molecular mechanism of honokiol on proliferation,migration and invasion of nasopharyngeal carcinoma cells(HK1 and CNE2).Methods CCK-8 kit was used to detect the activity of HK1 and CNE2 cells,colony forming test was used to detect the growth of HK1 and CNE2 cells,and Caspase-3 activity kit was used to detect the Caspase-3 activity of HK1 and CNE2 cells.the migration and invasion ability of HK1 and CNE2 cells were detected by wound healing test and Transwell invasion test,respectively.The expression levels of N-cadherin mRNA and vimentin mRNA in HK1 and CNE2 cells were detected by real-time fluorescence quantitative PCR.Results The HK1 and CNE2 cells were treated with honokiol at concentrations of 20,40,80μM for 24 and 48 h,the cells activity were lower than those of the control group(P<0.05).Compared with the control group,40μM honokiol could inhibite the colony formation of HK1 and CNE2 cells,and increased the activity of Caspase-3 in HK1 and CNE2 cells,reduce the wound healing rate and invasion number of HK1 and CNE2 cells,down regulated the expression of N-cadherin mRNA and vimentin mRNA in HK1 and CNE2 cells(P<0.05).Conclusion Honokiol can inhibit the proliferation,migration and invasion of nasopharyngeal carcinoma cells by promoting apoptosis and inhibiting epithelial mesenchymal transition.
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