contributes to the metastasis phenotype in human non-small-cell lung cancer cells possibly through the interaction with and .

BACKGROUND

Non-small-cell lung cancer (NSCLC) constitutes the leading cause of cancer death in humans. Previous studies revealed the essential role of the protein arginine methyltransferase 7 () in promoting metastasis in breast cancer. However, its function and potential mechanism in NSCLC remain unclear.

MATERIALS AND METHODS

The gene expression of between lung cancer tissues and normal tissues was studied with online database (http://medicalgenome.kribb.re.kr/GENT/). NSCLC cell lines with specific gene overexpression were constructed with lentivirus transduction. Matrigel invasion and colony formation assays were performed to evaluate the invasion and colony formation abilities. Co-immunoprecipitation coupled with mass spectrometry analysis was performed to explore the potential interaction proteins of . Bioinformatic analysis was performed with Gene Ontology and Kyoto Encyclopedia of Genes and Genomes databases.

RESULTS

Online analysis of gene expression patterns revealed the relatively high expression of in lung cancer tissues. overexpression was able to promote the invasion and colony formation of A549 and SPC-A1 cells. A total of 19 in-common proteins shared by both NSCLC cell lines were identified to be interacting with and found to participate in a wide variety of pathways and protein-protein interactions according to bioinformatic analysis. Among them, and were further investigated for their essential roles in promoted NSCLC cell invasion.

CONCLUSION

Our results suggested overexpression was able to promote metastasis in NSCLC possibly through the interaction with and , which provides the potential mechanism of oncogenesis in lung cancer.