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miR‐194 suppresses high glucose‐induced non‐small cell lung cancer cell progression by targeting NFAT5

机译:miR-194通过靶向NFAT5抑制高葡萄糖诱导的非小细胞肺癌细胞进展

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Diabetes mellitus (DM) is linked to an increased risk of lung cancer; however, the exact molecular basis is unclear. We used a microarray method and found a group of microRNAs differently expressed in lung cancer cells at high or low glucose treatment. Among these, miR-194 changed significantly, which indicated further analysis. miR-194 was significantly downregulated in non-small cell lung cancer (NSCLC) cells cultured in high glucose (HG) medium and clinical NSCLC tissues with DM. The introduction of miR-194 significantly suppressed the proliferation, migration, and invasion of lung cancer cells induced by HG, suggesting that miR-194 may be a suppressor during HG-induced NSCLC progression. Further analysis indicated that NFAT5 was a direct target gene of miR-194, evidenced by the direct binding of miR-194 with the 3'untranslated region of NFAT5. MiR-194 could decrease the expression of NFAT5 at both messenger RNA and protein levels, while overexpression of NFAT5 reversed the decreased proliferation, migration, and invasion ability mediated by miR-194 in lung cancer cells. Our findings provide new insight into the mechanism of NSCLC progression. Therapeutically, miR-194 may serve as a potential target for the treatment of lung cancer patients with DM. ? 2019 The Authors. Thoracic Cancer published by China Lung Oncology Group and John Wiley & Sons Australia, Ltd.
机译:糖尿病(DM)与肺癌的风险增加有关;但是,确切的分子基础尚不清楚。我们使用了微阵列方法,发现了一组在肺癌细胞中以高或低葡萄糖处理不同地表达的微小稻草。其中,MIR-194显着变化,表明进一步分析。 MiR-194在高葡萄糖(Hg)培养基和临床NMSCLC组织中培养的非小细胞肺癌(NSCLC)细胞中显着下调,用DM培养。 MiR-194的引入显着抑制了HG诱导的肺癌细胞的增殖,迁移和侵袭,表明MIR-194可以在HG诱导的NSCLC进展期间是抑制剂。进一步的分析表明,NFAT5是MIR-194的直接靶基因,通过MIR-194与NFAT5的3位转移区域直接结合证明。 MiR-194可以降低NFAT5在信使RNA和蛋白质水平的表达,而NFAT5的过度表达逆转MIR-194在肺癌细胞中介导的降低降低,迁移和侵袭能力。我们的调查结果为NSCLC进展的机制提供了新的洞察力。治疗上,miR-194可以作为治疗DM肺癌患者的潜在靶标。 ? 2019年的作者。中国肺部肿瘤集团和约翰瓦里和儿子澳大利亚发表的胸癌

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