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作 者:莫志洋 李英 韩晓东[1] 王虹霞[2] 翁巧凤 MO Zhiyang;LI Ying;HAN Xiaodong;WANG Hongxia;WENG Qiaofeng(Maxillofacial Plastic Surgery,Qinghai Provincial People′s Hospital,Xining 810008,China)
机构地区:[1]青海省人民医院颌面整形外科,西宁810008 [2]青海省人民医院麻醉科,西宁810008 [3]青海大学附属医学院口腔科,西宁810001
出 处:《实用医学杂志》2020年第22期3069-3073,共5页The Journal of Practical Medicine
基 金:青海省科技计划项目(编号:2017⁃ZJ⁃736)。
摘 要:目的观察淫羊藿次苷Ⅱ(icariinⅡ,ICSⅡ)对舌鳞状细胞癌(tongue squamous cell carcinoma,TSCC)上皮⁃间质转化(epithelial⁃mesenchymal transition,EMT)的抑制作用,及其通过Notch1/PTEN/FAK通路的调控机制。方法取对数期Tca⁃8113细胞,随机分为空白组,ICSⅡ低、中、高剂量组。测定各组增殖抑制率,迁移、侵袭能力,Notch1、PTEN、FAK、p⁃FAK蛋白相对表达量。结果ICSⅡ低、中、高剂量组24、48、72 h增殖抑制率均呈上升趋势(P<0.05);空白组,ICSⅡ低、中、高剂量组迁移率呈降低趋势(P<0.05),每个视野穿膜细胞数呈减少趋势(P<0.05),Notch1蛋白相对表达量及p⁃FAK/FAK呈降低趋势(P<0.05),PTEN蛋白相对表达量呈升高趋势(P<0.05)。结论ICSⅡ可抑制TSCC EMT,且呈剂量依赖性,推测与该药物可下调Notch1表达、上调PTEN表达、抑制FAK磷酸化有关。Objective To study the inhibitional effect of the icariinⅡon epithelial⁃mesenchymal transition(EMT)in tongue squamous cell carcinoma(TSCC)and explore its regulation through Notch1/PTEN/FAK signaling pathway.Methods Tca⁃8113 cells in logarithmic phase were randomly divided into blank group and ICSⅡlow,middle,high⁃dose groups.The comparisons were made among the groups in terms of cell proliferation inhibition rate,cell migration,intervention ability,relative expression of Notch1,PTEN,FAK,p⁃FAK protein of each group.Results The proliferation inhibition rate of ICSⅡlow,medium,high⁃dose groups showed an upward trend at 24,48 and 72 hours(P<0.05).The mobility and the number of transmembrane cells per field,Notch1 protein relative expression and p⁃FAK/FAK of the blank group,ICSⅡlow,medium,high⁃dose groups showed a down⁃ward trend(P<0.05),of which the PTEN protein relative expression showed an increasing trend(P<0.05).Conclusion ICSⅡcan inhibit TSCC EMT in a dose⁃dependent manner,which is speculated to be related to the down⁃regulation of Notch1 expression,up⁃regulation of PTEN expression,and inhibition of FAK phosphorylation.
关 键 词:淫羊藿次苷 舌鳞状细胞癌 抑制 上皮⁃间质转化 Notch1/PTEN/FAK通路
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