Upregulated microRNA-143 inhibits cell proliferation in human nasopharyngeal carcinoma

The aim of the present study was to investigate the possible functions and mechanism of microRNA (miR)-143 in cell proliferation of human nasopharyngeal carcinoma (NPC). The expression of miR-143 in NPC cells and tissues was investigated using reverse transcription-quantitative polymerase chain reaction. Cell viability assay, colony formation assay and flow cytometry were used to examine the cell proliferative ability and tumorigenicity. The expression levels of p21^Cip1, p27^Kip1, cyclin D1, phosphorylated (p)-retinoblastoma protein (Rb), Rb and cyclin-dependent kinase (CDK) 6 were determined by western blotting. Luciferase assay was used to confirm whether CDK6 was a direct target of miR-143. miR-143 was downregulated in NPC cell lines and tissues. Overexpression of miR-143 in NPC CNE1 cells inhibited proliferation, tumorigenicity and cell cycle progression. Additionally, ectopic expression of miR-143 downregulated cyclin D1 and p-Rb expression, and upregulated p21^Cip1 and p27^Kip1 expression, which subsequently inhibited NPC cell proliferation. It was also observed that CDK6 was a direct target of miR-143, which downregulated CDK6 expression. CDK6 suppression by miR-143 was associated with dysregulated expression of p21^Cip1, p27^Kip1, cyclin D1 and p-Rb, thereby serving an essential role in NPC cell growth. Our findings suggest that miR-143 inhibits proliferation by targeting CDK6, and may aid to identify new targets for anti-oncomiRs.