MicroRNA-19a mediates gastric carcinoma cell proliferation through the activation of nuclear factor-κB

In gastric carcinoma, the nuclear factor-κB (NF-κB) signaling pathway is highly active, and the constitutive activation of NF-κB prompts malignant cell proliferation. MicroRNAs are considered to be important mediators in the regulation of the NF-κB signaling pathway. The present study predominantly focussed on the effects of microRNA (miR)-19a on NF-κB activation. Reverse transcription-quantitative polymerase chain reaction was used to quantify the relative levels of miR-19a in gastric carcinoma cells. MTT assays were used to determine the effect of miR-19a on cellular proliferation. To detect the activation of NF-κB, western blotting was performed to measure the protein levels of NF-κB and the products of its downstream target genes. To define the target genes, luciferase reporter assays were used. miR-19a was found to be markedly upregulated in gastric carcinoma cells. The overexpression of miR-19a resulted in proliferation and enhanced migratory capabilities of the MGC-803 gastric carcinoma cell line. The results of the western blot analysis demonstrated that the protein levels of p65 increased when the MGC-803 cells were transfected with miR-19a mimics. In addition, the downstream target genes of miR-19a, including intercellular adhesion molecule, vascular cell adhesion molecule and monocyte chemoattractant protein-1, were upregulated. The results of the luciferase assay indicated that IκB-α was the target gene of miR-19a. Therefore, the results of the present study suggested that miR-19a enhances malignant gastric cell proliferation by constitutively activating the NF-κB signaling pathway.