Objective To explore miR-362-3 p expression in laryngeal cancer tissues and its effect on migration of Hep2 cells. Methods miR-362-3 p expression in 50 pairs of tumor and adjacent normal tissues was detected by real-time PCR after sample collection. The relationships between miR-362-3 p expression and clinical pathological characteristics in patients with laryngeal cancer were analyzed.mi R-362-3 p mimic, inhibitor, and control microRNA were transfected into Hep-2 cells. Transfection efficiency was determined by real-time PCR. Wound-healing and transwell assays were used to evaluate Hep-2 migration. Results miR-362-3 p expression was significantly higher in cancer tissues than in adjacent normal tissues (P ＜ 0.05). miR-362-3 p expression was statistically significantly related to node metastasis and clinical stage. Transfection with miR-362-3 p mimic and inhibitor significantly increased and decreased Hep-2 cell migration, respectively (both P ＜ 0.05). Conclusion miR-362-3 p is up-regulated in laryngeal cancer tissues and promotes laryngeal cancer cell migration, suggesting that it acts as a potential oncogene in laryngeal cancer.

Objective To study the mechanisms by which IL-4 inhibits formation of nod-like receptor protein 3 (NLRP3) inflammasome mediated by high mobility group box-1 (HMGB1) in microglia.Methods After the primary microglia were cultured at the gradient concentrations of HMGB1 (100,200 and 400 ng/mL) for 3 hours and extracted,the effects of HMGB1 on the NLRP3 inflammasome and on the expression of downstream transcription factor NF-κB were detected by immunofluorescence and Western Blotting.Meanwhile,BAY 11-7082,an NF-κB inhibitor,and IL-4 were added in HMGB1 to observe the changes in the NLRP3 inflammasome and NF-κB expression.Results HMGB1 significantly promoted the formation and expression of NLRP3 inflammasome components like NLRP3,ASC and Caspase-1 in microglia in a concentration-dependent manner (P＜0.05).This effect was inhibited by BAY 11-7082.The levels of relative protein expression of NLRP3,ASC and Caspase-1 in the group of 400 ng/mL HMGB1+BAY were significantly lower than in the group of 400 ng/mL HMGB1 (P＜0.05).At the same time,IL-4 significantly decreased the formation of NLRP3 inflammasome induced by HMGB1.The levels of relative protein expression of NLRP3,ASC and Caspase-1 in the group of 400 ng/mL HMGB1+IL-4 were significantly lower than in the group of 400 ng/mL HMGB1 (P＜0.05).Further finding demonstrated that IL-4 inhibited the activity of NF-κB in microglia.Conclusions HMGB1 may promote formation ofNLRP3 inflammasome via activating the NF-κB in microglia;IL-4 may inhibit formation ofNLRP3 inflammasome mediated by HMGB1 through negative regulation of NF-κB activity.