Identification of ELAVL1 gene and miRNA-139-3p involved in the aggressiveness of NSCLC.

OBJECTIVE

Tumor metastasis remains the main cause for the cancer-associated death of human non-small-cell lung carcinoma (NSCLC). Many studies have verified that microRNAs (miRNAs) exert crucial functions in the development of NSCLC. Nevertheless, the functions of miR-139-3p in NSCLC remain unexplored.

PATIENTS AND METHODS

The quantitative Real Time-PCR (qRT-PCR) assay was applied to assess the level of miR-139-3p and ELAV like RNA binding protein 1 (ELAVL1) in NSCLC tissues and cell lines. The growth of NSCLC cell was analyzed using 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium (MTS) assay and colony formation assay. The migration ability and invasiveness of NSCLC cells were analyzed using wound healing and transwell invasion analysis. The expression of ELAVL1 was determined by immunoblotting assay. The growth of NSCLC cell in vivo was assessed using xenograft model.

RESULTS

We uncovered that miR-139-3p was down expressed in NSCLC. MiR-139-3p repressed NSCLC cell growth, migration as well as invasion in vitro, and suppressed the progression of NSCLC cell in vivo. Mechanistically, ELAVL1 was proved as a downstream target of miR-139-3p. The level of ELAVL1 was upregulated in NSCLC and inversely associated with miR-139-3p level. Immunoblotting assay suggested that ELAVL1 was negatively modulated by miR-139-3p in NSCLC cell. In vivo, miR-139-3p repressed NSCLC cell growth and metastasis. Several recuse assays revealed that ELAVL1 mediated the inhibitory actions of miR-139-3p on the growth and metastatic-related traits of NSCLC cell.

CONCLUSIONS

Our results indicate that miR-139-3p acts as a suppressor in modulating the aggressiveness of NSCLC via regulating ELAVL1.