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首页> 外文期刊>Thoracic cancer. >Persistence of smoking induced non‐small cell lung carcinogenesis by decreasing ERBB pathway‐related microRNA expression
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Persistence of smoking induced non‐small cell lung carcinogenesis by decreasing ERBB pathway‐related microRNA expression

机译：通过降低erbB途径相关的微稻草表达，吸烟诱导的非小细胞肺癌患者的持久性

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Tobacco use is responsible for approximately 80-90% of non-small cell lung cancer cases. A large evidence base has shown that the ERBB pathway is associated with the occurrence of lung cancer. However, the mechanisms of how smoking activates the ERBB pathway have yet to be explained. We hypothesized that microRNAs may induce ERBB pathway activity during the process of lung cancer carcinogenesis. We analyzed microRNA array data from the Gene Expression Omnibus and the Kyoto Encyclopedia of Genes and Genomes to determine any associations between genes and smoking in three groups of patients with NSCLC: smokers, former smokers, and non-smokers. The interaction network among miRNAs, including hsa-mir-185-3p, hsa-mir-4295, hsa-mir-4288, and hsa-mir-613, promotes lung cancer development by affecting the ERBB pathway. Our findings provide evidence to explain the mechanism of lung cancer development in smokers. ? 2019 The Authors. Thoracic Cancer published by China Lung Oncology Group and John Wiley & Sons Australia, Ltd.
机译：烟草使用负责约80-90％的非小细胞肺癌病例。一个大的证据基础表明，ERBB途径与肺癌的发生有关。然而，尚未解释吸烟的机制激活ERBB途径。我们假设MicroRNAS可以在肺癌癌发生过程中诱导ERBB途径活动。我们分析了来自基因表达的MicroRNA阵列数据，以及基因和基因组的Kyoto百科全书，以确定基因和吸烟在三组NSCLC患者中的任何关联：吸烟者，前吸烟者和非吸烟者。 MIRNA中的相互作用网络，包括HSA-MIR-185-3P，HSA-MIR-4295，HSA-MIR-4288和HSA-MIR-613，通过影响ERBB途径来促进肺癌发育。我们的调查结果提供了证据来解释吸烟者肺癌发育的机制。 ？ 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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