High Metastasis-Associated Lung Adenocarcinoma Transcript 1 (MALAT1) Expression Promotes Proliferation, Migration, and Invasion of Non-Small Cell Lung Cancer via ERK/Mitogen-Activated Protein Kinase (MAPK) Signaling Pathway

BACKGROUND: In present study, we explored the function of the metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) gene in the development of non-small cell lung cancer (NSCLC). MATERIAL/METHODS: qRT-PCR was used to detect the MALAT1 mRNA expression level in cancer tissues and adjacent normal tissues of 115 NSCLC patients and in cell lines. MALAT1-mimic, MALAT1-inhibitor, and corresponding negative controls (NC) were utilized to transfect the H460 cells. Proliferation, migration, and invasion of H460 cells were evaluated by MTT method and Transwell assay. Expression levels of proteins in the ERK/MAPK signaling pathway were assessed by Western blot analysis. RESULTS: MALAT1 mRNA was upregulated in NSCLC tissues and cell lines compared to that in adjacent tissues and normal human bronchial cell line (BEAS-2B), respectively. Overexpression of MALAT1 significantly strengthened the proliferation, migration, and invasion ability of H460 cells. In comparison with the NC group, expression levels of CXCL5 and p-JNK proteins were elevated, while p-MAPK and p-ERK proteins were decreased in the MALAT1-mimic group. MALAT1 targets the 3′-untranslated region (UTR) fragment of the CXCL5 gene and inhibits its translation. Disturbance of the CXCL5 gene can reduce the protein expression of MAPK, p-MEK1/2, p-ERK1/2, and p-JNK, and inhibit the proliferation, migration, and invasion of MALAT1-mimic cells. CONCLUSIONS: High MALAT1 expression promotes the proliferation, migration, and invasion of non-small cell lung cancer via the ERK/MAPK signaling pathway.