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首页> 外文期刊>Oncology Research >Ran GTPase Induces EMT and Enhances Invasion in Non-Small Cell Lung Cancer Cells Through Activation of PI3K-AKT Pathway
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Ran GTPase Induces EMT and Enhances Invasion in Non-Small Cell Lung Cancer Cells Through Activation of PI3K-AKT Pathway

机译:Ran GTPase通过激活PI3K-AKT途径诱导EMT并增强非小细胞肺癌细胞的侵袭

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摘要

Ras-related nuclear protein (Ran) GTPase is upregulated in non-small cell lung cancer (NSCLC) cells and is required for NSCLC cell survival. However, the effect of Ran on NSCLC cell invasion and epithelial to mes-enchymal transition (EMT) remains unclear. This study found that Ran expression was much higher in highly invasive NSCLC cells than in lowly invasive NSCLC cells. Ectopic expression of Ran enhanced invasion and induced EMT in NSCLC cells. Inhibition of the PI3K-AKT pathway by LY294002, but not the MEK-ERK pathway by PD98509, reversed the above effects in these cells induced by Ran overexpression. In conclusion, our findings demonstrate that Ran induces EMT and enhances invasion in NSCLC cells through the activation of PI3K-AKT signaling. Thus, Ran may be a potential target for NSCLC therapeutic intervention.
机译:Ras相关的核蛋白(Ran)GTPase在非小细胞肺癌(NSCLC)细胞中上调,是NSCLC细胞存活所必需的。然而,Ran对NSCLC细胞侵袭和上皮向间质转化(EMT)的影响尚不清楚。这项研究发现,Ran表达在高侵袭性NSCLC细胞中比在低侵袭性NSCLC细胞中高得多。 Ran的异位表达增强了NSCLC细胞的侵袭并诱导了EMT。 LY294002抑制PI3K-AKT途径,而PD98509抑制MEK-ERK途径,却逆转了Ran过表达诱导的这些细胞的上述作用。总之,我们的发现表明Ran可以通过激活PI3K-AKT信号传导来诱导EMT并增强NSCLC细胞的侵袭性。因此,Ran可能是NSCLC治疗干预的潜在靶标。

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