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作 者:延青[1] 杨花荣[1] 王娜娜[1] YAN Qing;YANG Hua-rong;WANG Na-na(Department of Rhinolaryngology,Affiliated Hospital of Yan'an University,Yan'an Shaanxi 716000,China)
机构地区:[1]延安大学附属医院鼻咽喉科,陕西延安716000
出 处:《局解手术学杂志》2023年第9期778-782,共5页Journal of Regional Anatomy and Operative Surgery
基 金:延安市科技计划项目(2016HM-04-06)。
摘 要:目的探讨迷迭香酸(RA)对喉鳞状细胞癌(LSCC)细胞增殖、迁移的影响,并分析其潜在机制。方法取对数生长期的Hep-2和TU686细胞,分为对照组(未处理的Hep-2和TU686细胞)、低剂量组(20μmol/L的RA处理)、中剂量组(50μmol/L的RA处理)、高剂量组(100μmol/L的RA处理)、胰岛素生长因子1(IGF-1)组(10 nmol/mL IGF-1处理)、IGF-1+RA组(100μmol/L的RA与10 nmol/mL IGF-1同时处理)。倒置显微镜观察各组Hep-2和TU686细胞形态;CCK-8法检测各组Hep-2和TU686细胞增殖能力;细胞划痕实验检测各组Hep-2和TU686细胞迁移能力;Western blot检测各组Hep-2和TU686细胞中Ki-67、MMP-2、MMP-9及PI3K/AKT/mTOR信号通路相关蛋白的表达。结果RA可显著抑制Hep-2和TU686细胞的增殖、迁移,降低Ki-67、MMP-2、MMP-9蛋白表达和p-PI3K/PI3K、p-AKT/AKT、p-mTOR/mTOR水平(P<0.05);IGF-1可有效逆转RA对Hep-2和TU686细胞增殖、迁移以及PI3K/AKT/mTOR信号通路的抑制作用(P<0.05)。结论RA可能通过PI3K/AKT/mTOR信号通路抑制LSCC细胞的增殖和迁移。Objective To investigate the effect of rosmarinic acid(RA)on the proliferation and migration of laryngeal squamous cell carcinoma(LSCC)cells,and analyze its underlying mechanism.Methods Hep-2 and TU686 cells in logarithmic growth phase were taken and divided into control group(untreated Hep-2 and TU686 cells),low-dose group(treated with 20μmol/L RA),middle-dose group(treated with 50μmol/L RA),high-dose group(treated with 100μmol/L RA),insulin-like growth factor 1(IGF-1)group(treated with 10 nmol/L IGF-1)and IGF-1+RA group(co-treated with 100μmol/L RA and 10 nmol/mL IGF-1).Inverted microscope was used to observe the morphology of Hep-2 and TU686 cells in each group;CCK-8 method was used to detect the proliferation of Hep-2 and TU686 cells in each group;scratch wound healing assay was used to detect the migration ability of Hep-2 and TU686 cells in each group;Western blot was used to detect the expression of Ki-67,MMP-2,MMP-9 and PI3K/pAKT/mTOR signaling pathway-related proteins in Hep-2 and TU686 cells of each group.Results RA could significantly inhibit the proliferation and migration of Hep-2 and TU686 cells,reduce the protein expression of Ki-67,MMP-2,MMP-9 and the levels of p-PI3K/PI3K,p-AKT/AKT,and p-mTOR/mTOR(P<0.05);IGF-1 could effectively reverse the inhibitory effect of RA on Hep-2 and TU686 cell proliferation,migration and PI3K/AKT/mTOR signaling pathway(P<0.05).Conclusion RA may inhibit the proliferation and migration of LSCC cells through PI3K/AKT/mTOR signaling pathway.
关 键 词:迷迭香酸 PI3K/AKT/mTOR信号通路 喉鳞状细胞癌 细胞增殖 细胞迁移
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