Introduction: Laryngeal squamous cell carcinoma (LSCC) is a highly aggressive malignant cancer, but the molecular mechanisms underlying its development and progression remain largely elusive. The purpose of the present study is to investigate the expression profile and functional role of microRNA-625 (miR-625) in LSCC.Materials and methods: LSCC tissues and adjacent normal tissues were collected from 86 LSCC patients. The expression levels of miR-625 and SOX4 mRNA in tissues and cells were detected by RT-qPCR analysis. The expression levels of SOX4 and EMT-related proteins were detected by western blot analysis. In vitro cell proliferation, migration, and invasion were detected by MTT assay, colony formation assay, wound healing assay, and transwell invasion assay, respectively. Dual-luciferase reporter assay was performed to verify the binding relationship between miR-625 and the 3′-UTR of SOX4.Results: The results demonstrated that miR-625 is significantly down-regulated in clinical LSCC tissues, and its low expression may be closely associated with unfavorable clinicopathological characteristics of LSCC patients. Overexpression of miR-625 significantly suppressed the proliferation, migration, invasion, and EMT of LSCC cells. Furthermore, SOX4 was validated as a direct target of miR-625 in LSCC cells, and rescue experiments suggested that restoration of SOX4 blocked the tumor suppressive role of miR-625 in LSCC cells.Conclusions: Taken together, these findings highlighted a critical role of miR-625 in the pathogenesis of LSCC, and restoration of miR-625 could be considered as a potential therapeutic strategy against this fatal disease.
The effectiveness of acupuncture in the treatment of dry eye has been confirmed, but the association between acupoint selection and therapeutic effect has remained to be elucidated. In the present study, a systematic review and meta-analysis were performed to evaluate the effect of periocular acupoints and periocular acupoints plus body acupoints compared with AT for the treatment of dry eye disease (DED). The PubMed, Cochrane Library, Embase, Ovid, China National Knowledge Infrastructure and Chonqing VIP Information, Co., Ltd. databases were searched with entries until 10 July 2018 considered. Only randomized controlled trials (RCTs) were included. Meta-analyses were performed to compare the effects of acupuncture with those of conventional treatment (including AT or other non-acupuncture therapies). The primary outcomes, including tear break-up time (BUT), Schirmer's I test (SIT) result and Symptom scores were analyzed. Subgroup analysis was performed for periocular acupoints only and periocular acupoints plus body acupoints. A total of 12 studies comprising 900 participants were included. In the primary meta-analysis, a significant improvement in the BUT [n=1,209, weighted mean difference (WMD)=1.01, 95% CI: 0.56-1.84, P<0.00001], SIT result (n=1,107, WMD=1.98, 95% CI: 0.44-3.34, P<0.00001) and Symptom scores (n=402, WMD=-1.02, 95% CI:-1.33 to-0.72, P<0.00001) was obtained to evaluate the clinical efficacy of acupuncture and AT. Furthermore, periocular acupoints plus body acupoints were more effective in the treatment of DED. However, the total sample size of subjects with only periocular acupoints in the treatment of DED was too small to get any firm conclusions. Further large RCTs are warranted.
Purpose. We tried to investigate whether electroacupuncture (EA) can reduce inflammation of dry eye disease (DED) by regulating α7nAChR and inhibiting the NF-κB signaling pathway. Methods. Healthy New Zealand white rabbits were treated with scopolamine hydrobromide (Scop) for 21 consecutive days to establish the DED animal model. After 21 days, EA, fluorometholone (Flu), and α7nAChR antagonist (α-BGT) treatments were performed, and the Scop injection was continued until day 35. During treatment, the fluorescence staining of the corneal epithelium and the level of tear flow were observed. The influence of EA on the LG pathology and inflammatory factors ACh, α7nAChR, and NF-κB was detected using the LG histopathology, transmission electron microscopy (TEM), cytokine protein chip technology, enzyme-linked immunosorbent assay (ELISA), and Western blot. Results. The EA stimulation can reduce the corneal epithelial damage and repair epithelial cell ultrastructure, promote the tear secretion, relieve the LG atrophy and decrease lipid droplet accumulation in LG acinar cell, and reduce the levels of inflammatory cytokines (i.e., IL-1, MIP-1b, TNF-α, and IL-8) in the LG. The protective effect of EA on the inflammation and the ocular surface is similar to the corticosteroid Flu. EA and Flu can upregulate the expression of the α7nAChR and downregulate the expression of NF-κB. The α7nAChR antagonist α-BGT can reverse the protective effect of EA on the LG and the inhibitory effect on the NF-κB pathway and the expression of inflammatory factors but cannot affect the expression of Flu on the NF-κB pathway and inflammatory factors. Conclusion. These results prove that EA can alleviate DEDs by stimulating the acupoints around the eyes. These beneficial effects are related to the upregulation of α7nAChR and the downregulation of NF-κB in the LG. The protective effect of LG is mediated through the anti-inflammatory pathway mediated by α7nAChR. EA can reduce the NF-κB P65 nuclear transcription and reduce inflammatory factors by regulating α7nAChR. This expression indicates that the α7nAChR/NF-κB signaling pathway may serve as a potential therapeutic target for EA to treat DEDs.
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