MicroRNA‑200a mediates nasopharyngeal carcinoma cell proliferation through the activation of nuclear factor‑κB

Abstract In nasopharyngeal carcinoma (NPC), the nuclear factor‑κB (NF‑κB) signaling pathway is highly active. The constitutive activation of NF‑κB prompts malignant cell proliferation, and microRNAs are considered an important mediator in regulating the NF‑κB signaling pathway. The current study investigated the effect of microRNA‑200a (miR‑200a) on NF‑κB activation. Reverse transcription‑quantitative polymerase chain reaction was used to quantify the relative level of miR‑200a in NPC tissue samples and CNE2 cells. An MTT assay was used to investigate the effect of miR‑200a on cell proliferation. To investigate the activation of NF‑κB, western blotting was used to measure the protein levels of NF‑κB and its downstream targets. To identify the target genes of miR‑200a, a luciferase reporter assay was used. The current study demonstrated that miR‑200a was upregulated in NPC tissue samples and cell lines. Overexpression of miR‑200a resulted in the proliferation of CNE2 cells. Western blot analysis indicated that the protein levels of p65 increased when CNE2 cells were transfected with miR‑200a mimics. Additionally, the downstream targets of miR‑200a were upregulated, including vascular cell adhesion molecule, intercellular adhesion molecule and monocyte chemoattractant protein‑1. The luciferase assay indicated that IκBα was the target gene of miR‑200a. In conclusion, miR‑200a was demonstrated to enhance NPC cell proliferation by activating the NF‑κB signaling pathway.