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miR-646 is a key negative regulator of EGFR pathway in lung cancer

机译:miR-646是肺癌中EGFR通路的关键负调控因子

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Background: As one of the leading cause of cancer-related deaths in the worldwide, lung cancer needs to be understood better. Nowadays, increasing point mutations of specific oncogenes are biomarkers used to predict the therapeutic effect of targeted therapy and lung cancer has entered the age of individual treatment. At present, many relevant researchers have suggested that EGFR is a biomarker used to predict the therapeutic effect of targeted therapy. A large number of evidence indicates that EGFR/Akt pathway plays important role in cancer growth and metastasis. Aim of the Study: In this paper, we found EGFR was a target of miR-646. Results: Overexpression of miR-646 not only downregulated EGFR/Akt pathway, but also inhibited lung cancer cell proliferation and metastasis. At the same time, miR-646 was a prognosis factor for overall survival. Conclusion: Our finding could provide new insights into the molecular therapeutic of lung cancer.
机译:背景:作为全球癌症相关死亡的主要原因之一,人们需要更好地了解肺癌。如今,特定致癌基因的增加点突变是用于预测靶向治疗的治疗效果的生物标志物,肺癌已进入个体治疗时代。目前,许多相关研究人员提出,EGFR是一种生物标志物,可用于预测靶向治疗的疗效。大量证据表明,EGFR / Akt通路在癌症的生长和转移中起着重要的作用。研究目的:在本文中,我们发现EGFR是miR-646的靶标。结果:miR-646的过表达不仅下调了EGFR / Akt通路,而且抑制了肺癌细胞的增殖和转移。同时,miR-646是整体生存的预后因素。结论:我们的发现可以为肺癌的分子治疗提供新的见解。

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