Mucin 1 (MUC1) is a transmembrane glycoprotein that is aberrantly unregulated in numerous types of cancer, including non-small cell lung cancer (NSCLC), and serves a key role as an oncogene in the tumorigenesis of various human adenocarcinomas. Studies have indicated that MUC1 is involved in cell proliferation, invasion and migration. However, the role of MUC1 in NSCLC progression remains poorly understood. The aim of the present study was to investigate the role of MUC1 in stable MUC1-low-expression NSCLC cell lines that were generated by transfection with MUC1-siRNA. Cell Counting Kit-8 assay was preformed to determine the proliferation ability of NSCLC cells, while cell apoptosis was detected using flow cytometry. In addition, the mRNA and protein expression levels of MUC1 were detected by reverse transcription-quantitative polymerase chain reaction and western blot analysis, respectively. Western blot analysis was also used for detection of other associated proteins. The results demonstrated that, compared with the control group, the cell proliferation ability was significantly declined in the MUC1 inhibition group, and the cell apoptosis rate was markedly increased. Inhibition of MUC1 gene in NCI-H1650 cells suppressed cell proliferation and induced cell apoptosis. In addition, the protein expression levels of vascular endothelial growth factor (VEGF) and VEGF-C were notably decreased by MUC1 inhibition, indicating the anti-angiogenic effect of MUC1 downregulation. Furthermore, inhibition of MUC1 gene with MUC1-siRNA significantly suppressed the phosphorylation of protein kinase B and extracellular signal-regulated kinase. In conclusion, the findings indicated that silencing of MUC1 gene may inhibit the development of NSCLC cells.
Keywords: anti-angiogenic effect; apoptosis; mucin 1; non-small cell lung cancer; proliferation.