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.