首页> 外文期刊>Tumour biology : >MicroRNA-21 promotes cell proliferation, migration, and resistance to apoptosis through PTEN/PI3K/AKT signaling pathway in esophageal cancer
【24h】

MicroRNA-21 promotes cell proliferation, migration, and resistance to apoptosis through PTEN/PI3K/AKT signaling pathway in esophageal cancer

机译:MicroRNA-21通过PTEN / PI3K / AKT信号通路促进食管癌细胞增殖,迁移和对凋亡的抵抗

获取原文
获取原文并翻译 | 示例
           

摘要

Our study aimed to explore associations between microRNA-21 (miR-21) and PTEN/PI3K/AKT signaling pathway and, further, to elucidate the regulation of miR-21 on biological behaviors in human esophageal cancer cells. The expressions of miR-21, PTEN, PI3K, and AKT were detected in 89 esophageal cancer samples and 58 adjacent normal tissues respectively. The human esophageal cancer cells (TE11) were grouped as following: blank (TE11 cells without transfection), negative (TE11 cells with miR-21 negative inhibitor), and Inhibition-miR21 (TE11 cells with miR-21 inhibitor). Western blot was used for detection of PTEN, P13K, and AKT protein expressions, MTT method for cell proliferation, Transwell assay for cell migration and invasion, and flow cytometry for cell cycle and apoptosis. MiR-21, PI3K, and AKT have higher expressions, but PTEN has lower expression in esophageal cancer tissues compared with adjacent normal tissues. The esophageal cancer tissues with lymph node metastasis and poor differentiation showed significantly low positive rate of PTEN protein, but high positive rates of PI3K and AKT proteins. Compared with blank and negative groups, PTEN expression of TE11 cells in Inhibition-miR21 group was significantly up-regulated, but PI3K and AKT were down-regulated. Further, PTEN was a target gene of miR-21. Besides, compared with blank and negative groups, the proliferation, migration, and invasion of TE11 cells were less active in Inhibition-miR21 group. TE11 cells were significantly increased in the G0/G1 phase of cell cycles, but decreased in the S and G2/M phase in Inhibition-miR21 group. The TE11 cells exhibited significantly increased apoptosis rates. MiR-21 targets key proteins in PTEN/PI3K/AKT signal pathway, promoting proliferation, migration, invasion, and cell cycle, and inhibiting apoptosis of human esophageal cancer cells. It may serve as a novel therapeutic target in esophageal cancer.
机译:我们的研究旨在探讨microRNA-21(miR-21)与PTEN / PI3K / AKT信号传导途径之间的关联,并进一步阐明miR-21对人食道癌细胞生物学行为的调节。在89例食管癌标本和58例癌旁正常组织中检测到miR-21,PTEN,PI3K和AKT的表达。人食道癌细胞(TE11)分为以下几类:空白(未转染的TE11细胞),阴性(带有miR-21阴性抑制剂的TE11细胞)和抑制-miR21(带有miR-21抑制剂的TE11细胞)。 Western blot检测PTEN,P13K和AKT蛋白表达,MTT检测细胞增殖,Transwell检测细胞迁移和侵袭,流式细胞仪检测细胞周期和凋亡。与邻近的正常组织相比,MiR-21,PI3K和AKT在食管癌组织中的表达较高,但PTEN在食管癌组织中的表达较低。具有淋巴结转移和分化差的食道癌组织显示PTEN蛋白的阳性率明显较低,而PI3K和AKT蛋白的阳性率较高。与空白和阴性组相比,Inhibition-miR21组的TE11细胞PTEN表达明显上调,而PI3K和AKT下调。另外,PTEN是miR-21的靶基因。此外,与空白组和阴性组相比,Inhibition-miR21组的TE11细胞的增殖,迁移和侵袭活性较低。在抑制-miR21组中,TE11细胞在细胞周期的G0 / G1期显着增加,但在S和G2 / M期却降低。 TE11细胞表现出明显增加的凋亡率。 MiR-21靶向PTEN / PI3K / AKT信号通路中的关键蛋白,促进增殖,迁移,侵袭和细胞周期,并抑制人食道癌细胞的凋亡。它可以作为食道癌的新型治疗靶标。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号