MicroRNA-29 targets FGF2 and inhibits the proliferation, migration and invasion of nasopharyngeal carcinoma cells via PI3K/AKT signaling pathway

摘要

OBJECTIVE: Studies have indicated that miRNAs may prove essential therapeutic targets for the treatment of cancer. The study was designed to investigate the role and therapeutic potential of miR-29 in nasopharyngeal cancer. MATERIALS AND METHODS: The quantitative Real-time polymerase chain reaction (qRT-PCR) was used for expression analysis. WST-1 assay was used for cell viability assessment. The 4′,6-diamidino-2-phenylindole (DAPI) staining and electron microscopic analysis was used for the detection of apoptosis and autophagy, respectively. Transwell assays were used for cell migration and invasion assay. RESULTS: It was found that miR-29 is significantly downregulated in nasopharyngeal cancer cell lines. Overexpression of miR-29 causes decrease in the viability of CNE2 nasopharyngeal cancer cells via induction of apoptosis and autophagy. Bioinformatics analysis indicated FGF2 to be the target of miR-29 in CNE2 cells, which was also confirmed by luciferase reporter assay. The qRT-PCR results showed fibroblast growth factor 2 (FGF2) to be significantly upregulated in the nasopharyngeal cancer cell lines. However, miR-29 overexpression in CNE2 cells resulted in post-transcriptional suppression of FGF2 expression. Nonetheless, silencing of FGF2 also caused inhibition of CNE2 cell proliferation via induction of apoptosis and autophagy. Overexpression of FGF2 could reverse the effects of miR-29 overexpression on the proliferation of CNE2 cells. Moreover, overexpression of miR-29 causes significant decline in the phosphorylation of PI3K and AKT expression cells and inhibits their migration and invasion of the CNE2 cells. Finally, miR-29 overexpression could also suppress the subcutaneous xenografted tumor growth. CONCLUSIONS: The findings of the present study indicate the therapeutic implications of miR-29 in nasopharyngeal carcinoma.