Multiple MicroRNAs synergistically promote tolerance to epidermal growth factor receptor-targeted drugs in smoked lung cancer therapies.
Aims
Lung cancer is one of the leading causes of cancer-related mortality. Tobacco usage is considered as associated with the carcinogenesis, progression, and prognosis of lung cancer. Previous studies have demonstrated that the smoking inhibited medical therapy results from K-Ras gene mutation through suppressing the epidermal growth factor receptor (EGFR) pathway. However, recent clinical trials have revealed that few smoked lung cancer patients present K-Ras gene mutation; yet, the majority of smoked lung cancer patients remain K-Ras nonmutation. The chemo-resistant mechanism remains unclear. Recently, microRNA (miRNA) interaction has been found to play an important role in drug resistance process. We hypothesized that miRNA may exert medicine resistance during the processes of lung cancer therapy.


Methods
Here, we analyzed miRNA array data from the GEO database.


Results
Our results showed that the interaction network among hsa-miR-30d-3p, hsa-miR-184, hsa-miR-500a, hsa-miR-542-3p, among others, inhibited EGFR-targeted medicine therapy.


Conclusion
The research will provide evidence that promotes novel therapy of lung cancers.
['Pan|Li|L|', 'Wang|Hailong|H|', 'Jiang|Chengwen|C|', 'Li|Wei|W|', 'Chen|Yongzi|Y|', 'Ying|Guoguang|G|']
D014408:Biomarkers, Tumor D019008:Drug Resistance, Neoplasm D066246:ErbB Receptors D020869:Gene Expression Profiling D015972:Gene Expression Regulation, Neoplastic D053263:Gene Regulatory Networks D006801:Humans D008175:Lung Neoplasms D035683:MicroRNAs D011379:Prognosis D047428:Protein Kinase Inhibitors D055752:Small Cell Lung Carcinoma
microRNA smoking lung cancer Epidermal growth factor receptor