Open AccessPersistence of smoking induced non‐small cell lung carcinogenesis by decreasing ERBB pathway‐related microRNA expression
Author(s) -
Zhang Lianmin,
Wang Hailong,
Wang Changli
Publication year - 2019
Publication title -
thoracic cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.823
H-Index - 28
eISSN - 1759-7714
pISSN - 1759-7706
DOI - 10.1111/1759-7714.13020
Subject(s) - microrna , lung cancer , carcinogenesis , medicine , kegg , erbb , cancer research , lung , gene , gene expression , cancer , bioinformatics , oncology , genetics , biology , gene ontology
Background 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. Methods 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. Results 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. Conclusion Our findings provide evidence to explain the mechanism of lung cancer development in smokers.