In recent years, microRNAs (miRNAs/miRs) have gained increasing fascination with cancer research. miR-25-overexpressing NSCLC cells. Furthermore, it had been proven that miR-25 triggered the extracellular signal-regulated kinase (ERK) signaling pathway, which resulted in improved vimentin ultimately, matrix metalloproteinase 11 and N-cadherin amounts, as well as the downregulation of E-cadherin manifestation by inhibiting the manifestation of KLF4. To conclude, miR-25 was proven to activate the ERK signaling pathway by focusing on KLF4 straight, advertising cell invasion and migration. The results of today’s research indicated that miR-25 or KLF4 may provide as a restorative target for the treating NSCLC. (25) reported that upregulated miR-25 in liver organ cancer tissues resulted in a shorter success period. Li (26) also reported that overexpressed miR-25 improved the proliferation, invasion and Fenretinide migration of gastric tumor cells by causing the degradation of transducer of ERBB2 1 and in addition proven that serum concentrations of miR-25 had been positively connected with poor prognosis in individuals with gastric tumor. However, using diseases, miR-25 was downregulated. For instance, diminished expression of miR-25 in colorectal cancer induced an increase in expression of angiopoietin like 2 and resulted in reduced cell clones, inhibited invasion and migration (27). Furthermore, Wu (28) studied miR-25, which was reported to promote cell growth and inhibit apoptosis in Fenretinide NSCLC by reducing modulator of apoptosis 1 expression. Xiang (29) revealed that miR-25 was overexpressed in NSCLC cells and tissues, and promoted the motility and proliferation of NSCLC cells, in part by diminishing F-box and WD repeat domain containing 7 expression levels. The majority of studies have investigated the biological function of miR-25 in lung cancer, however the underlying mechanism is remains unknown. The aim of the present study was to research the function of miR-25 in NSCLC and to improve the understanding of the underlying mechanism of miR-25 in NSCLC. In the present study, the expression levels of miR-25 were examined in NSCLC tissues via reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Subsequently, assays, including cell migration and invasion assays, were conducted to understand the biological functions of miR-25 in NSCLC. Additionally, KLF4 was demonstrated to be a novel target gene of miR-25, and to be involved in the invasion and migration in NSCLC cells. Finally, the phosphorylation of extracellular signal-regulated kinase (ERK1/2; p44/42 mitogen-activated protein kinase) demonstrated that the ERK signaling pathway was downstream of miR-25. Collectively, the results of the present study revealed that miR-25 promoted the migration and CD52 invasion of NSCLC cells via Fenretinide regulation of Fenretinide the ERK1/2 signaling pathway by targeting KLF4. Materials and methods Tissue samples and cell lines Pairs of normal and NSCLC tissue specimens (n=31; 21 male and 10 female; age, 41C77) were obtained from patients that received surgery at the Cardiovascular Surgery of First Affiliated Hospital of Gannan Medical University (Ganzhou, China) between January 2014 and March 2016. Specimens were placed immediately into liquid nitrogen following collection and were then stored at ?80C until use. Written informed consent was obtained from the patients involved in Fenretinide the present study, which was approved by the Ethics Committee of Gannan Medical University. Human A549 and Calu1 NSCLC cell lines, GES-1 and 293T cells used in the present study were obtained from the Institute of Biochemistry and Cell Biology from the Chinese language Academy of Sciences (Shanghai, China), A549, 293T and GES-1 cells were cultured in.