MicroRNA-212-5p regulates the inflammatory response of periodontal ligament cells by targeting myeloid differentiation factor 88.

OBJECTIVE: This study was aimed to investigate the effects of microRNA-212-5p (miR-212-5p) and myeloid differentiation factor 88 (Myd88) in Porphyromonas gingivalis lipopolysaccharide (P. gingivalis LPS)-challenged human periodontal ligament cells (PDLCs). METHODS: The levels of miR-212-5p and Myd88 in PDLCs were determined via quantitative real-time Polymerase Chain Reaction. Cell viability and pro-inflammatory cytokines were assessed using MTT assay and enzyme-linked immunosorbent assay. Bioinformatics and luciferase reporter gene assay were employed to explore the interaction between miR-212-5p and Myd88. Moreover, the activation of p38 mitogen-activated protein kinase (MAPK) and nuclear factor kappa-B signal pathways were testified via western blot analysis. RESULTS: MiR-212-5p was downregulated following stimulation of P. gingivalis LPS. Overexpression of miR-212-5p elevated the cell viability and reduced the secretion of pro-inflammatory cytokines. Myd88 is a target of miR-212-5p. Notably, pcDNA3.1-Myd88 reversed the anti-inflammatory effect of miR-212-5p overexpression. Likewise, miR-212-5p mimic inhibited the activation of p38 MAPK and nuclear factor kappa-B, whereas pcDNA3.1-Myd88 abrogated the effect of miR-212-5p mimic. CONCLUSIONS: MiR-212-5p inhibited the inflammatory response in PDLCs by targeting Myd88, which may involve the inactivation of p38 MAPK and nuclear factor kappa-B.

Effects of KIF2A on the prognosis of nasopharyngeal carcinoma and nasopharyngeal carcinoma cells.

Nasopharyngeal carcinoma (NPC) is a common tumor in south China. Kinesin family member 2A (KIF2A) belongs to the kinesin-13 family and is associated with the growth and invasion of a number of different types of human cancer, including ovarian, breast and prostate cancer. The aim of the present study was to evaluate the expression of KIF2A in NPC and explore the relationship between KIF2A and the basic characteristics of 5-8F cells. Immunohistochemistry was performed on tissues from 97 patients with NPC to assess KIF2A protein expression. KIF2A was knocked down by a specific short interfering (si)RNA in 5-8F cell lines. Cell proliferation, apoptosis and cycle were analyzed by MTT assay and flow cytometry. The invasive ability and angiogenesis were evaluated by Matrigel assay and reverse transcription-quantitative PCR. The level of KIF2A was associated with the growth and migration of primary tumor, nodal status and tumor stage. The viability of KIF2A-knockdown cells was decreased compared with that of the control cells. The number of apoptotic cells, as well as the percentage of cells in the G0/G1 phase, was higher in the KIF2A siRNA group compared with the control group. The invasive and angiogenetic ability of 5-8F cells in the KIF2A siRNA group was decreased compared with the control group. In conclusion, the expression of KIF2A correlated with the poor clinicopathological features in NPC. Therefore, KIF2A may serve an important role in the progression of NPC and proliferation of 5-8F cells, which might present a potential therapeutic target for patients with NPC.