双荧光素酶报告基因分析证明miR-616-5p是AP000892.6的靶基因(P<0.01).与NC组比较,AP000892.6对miR-616-5p表达具有负调控作用(P<0.01).与NC组比较,AP000892.6组T24细胞中上皮表型蛋白E-cadherin,ZO-1表达上调,间充质表型蛋白Vimentin,N-cadherin,Twist表达下调.结论AP000892.6通过靶向miR-616-5p抑制膀胱癌T24细胞...
双荧光素酶报告基因分析证明miR-616-5p是AP000892.6的靶基因(P<0.01).与NC组比较,AP000892.6对miR-616-5p表达具有负调控作用(P<0.01).与NC组比较,AP000892.6组T24细胞中上皮表型蛋白E-cadherin,ZO-1表达上调,间充质表型蛋白Vimentin,N-cadherin,Twist表达下调.结论AP000892.6通过靶向miR-616-5p抑制膀胱癌T24细胞...
Sulforaphane suppresses EMT and metastasis in human lung cancer through miR-616-5p-mediated GSK3beta/beta-catenin signaling pathways. Acta Pharmacol Sin 2016;Wang DX, Zou YJ, Zhuang XB, Chen SX, Lin Y, Li WL, Lin JJ and Lin ZQ. Sulforaphane suppresses EMT and metastasis in human lung ...
In fresh NSCLC tissue samples from 179 patients, miR-616-5p levels were upregulated in late-stage NSCLCs, and strongly correlated with risk of NSCLC recurrence and metastasis. Consistent with the clinic observation, miR-616-5p levels in the 3 NSCLC cell lines were correlated with their ...
Silencing miR-616-5p markedly suppressed the migration and invasion of 95D cells in vitro and NSCLC metastasis in vivo. Further studies revealed that miR-616-5p directly targeted GSK3β and decreased its expression, whereas sulforaphane decreased miR-616-5p levels by histone modification, and ...
它控制各种各样的癌症的 tumorigenesis 或前进展出有效反癌症行动.最近的研究证明了 sulforaphane 稀释在非小的房间肺癌症(NSCLC ) 表明小径的 EGFR,建议它的潜在的反变形的效果.在这研究,我们在上皮间充质的转变(EMT ) 和 NSCLC 转移估计了 sulforaphane 和 miR-616-5p 的参与.Sulforaphane 与 9.52 桳睯琠慨 ?
Sulforaphane suppresses EMT and metastasis in human lung cancer through miR-616-5p-mediated GSK3beta/beta-catenin signaling pathways. Acta Pharmacol Sin 2016;Wang DX, Zou YJ, Zhuang XB, Chen SX, Lin Y, Li WL, Lin JJ and Lin ZQ. Sulforaphane suppresses EMT and metastasis in human lung ...
Downregulation of long noncoding RNA TUSC7 promoted cell growth, invasion and migration through sponging with miR-616-5p/GSK3β pathway in ovarian cancerZHU, L.-M.LI, N.European Review for Medical & Pharmacological Sciences