miR-150 promotes the proliferation and migration of lung cancer cells by targeting SRC kinase signalling inhibitor 1.

microRNAs (miRNAs) are a class of endogenously expressed, small non-coding RNAs that play an important role in the regulation of gene expression at the post-transcriptional level. Dysregulation of miRNAs is associated with a variety of diseases, including lung cancer. In the present study, miR-150 was found to be significantly upregulated in lung cancer clinical specimens by quantitative real-time polymerase chain reaction (RT-PCR). Using bioinformatics analysis, v-src avian sarcoma (Schmidt-Ruppin A-2) viral oncogene homolog (SRC) kinase signalling inhibitor 1 (SRCIN1), an important regulator of SRC activity, was predicted to be a potential target of miR-150. Furthermore, an inverse correlation between miR-150 and SRCIN1 protein levels, but not mRNA levels, was identified in human lung cancer tissue samples. By overexpressing or knocking down miR-150 in lung adenocarcinoma A549 cells and H1975 cells, it was experimentally validated that miR-150 is a direct regulator of SRCIN1. It was further confirmed that miR-150 directly recognises the 3'-untranslated region (3'-UTR) of SRCIN1 transcript with a luciferase reporter assay. Finally, it was demonstrated that the repression of SRCIN1 by miR-150 consequently triggered the activation of the Src/focal adhesion kinase (FAK) and Src/Ras/extracellular signal-regulated kinase (ERK) pathway, which eventually promoted the proliferation and migration of A549 cells, and this promotion by miR-150 could be reversed by overexpressing SRCIN1. Taken together, our findings provide the first clues regarding the role of miR-150 as an oncogene in lung cancer through the inhibition of SRCIN1 translation.