Identification of core gene in chronic rhinosinusitis with nasal polyps and correlations with inflammation-related genes.

OBJECTIVE: Our aim in this study is to identify the core genes of chronic rhinosinusitis with nasal polyps and analyze the correlations between it and inflammation-related genes. METHODS: GSE72713 dataset containing gene expression data of ECRSwNP, nonECRSwNP and healthy samples was obtained from Gene Expression Omnibus (GEO) and filtered by limma to identify DEGs among three groups, then the functions and correlated pathways of DEGs were analyzed using GO and KEGG. The core DEGs were selected by the intersection of DEGs and the PPI network was constructed via STRING. The correlations between the expression levels of CRSwNP core gene and inflammation-related genes were analyzed via the Mann-Whitney U test. RESULTS: The DEGs among ECRSwNP, nonECRSwNP, and CTRL were filtered respectively, and enrichment analysis showed they were associated with olfaction and/or immune responses. The PPI network was constructed by 7 core DEGs obtained via the intersection among three groups, and ALOX15 was confirmed as the core gene in the network. Subsequently, the correlations between the expression levels of ALOX15 and inflammation-related genes were illustrated. CONCLUSION: In this study, the core gene ALOX15 was selected from the DEGs among ECRSwNP, nonECRSwNP, and CTRL. IL5, IL1RL1, and IL1RAP were found to exhibit a significant positive correlation with ALOX15. LEVEL OF EVIDENCE: Level 3.

Identification of core gene in chronic rhinosinusitis with nasal polyps and correlations with inflammation-related genes

Abstract Objective Our aim in this study is to identify the core genes of chronic rhinosinusitis with nasal polyps and analyze the correlations between it and inflammation-related genes. Methods GSE72713 dataset containing gene expression data of ECRSwNP, nonECRSwNP and healthy samples was obtained from Gene Expression Omnibus (GEO) and filtered by limma to identify DEGs among three groups, then the functions and correlated pathways of DEGs were analyzed using GO and KEGG. The core DEGs were selected by the intersection of DEGs and the PPI network was constructed via STRING. The correlations between the expression levels of CRSwNP core gene and inflammation-related genes were analyzed via the Mann-Whitney U test. Results The DEGs among ECRSwNP, nonECRSwNP, and CTRL were filtered respectively, and enrichment analysis showed they were associated with olfaction and/or immune responses. The PPI network was constructed by 7 core DEGs obtained via the intersection among three groups, and ALOX15 was confirmed as the core gene in the network. Subsequently, the correlations between the expression levels of ALOX15 and inflammation-related genes were illustrated. Conclusion In this study, the core gene ALOX15 was selected from the DEGs among ECRSwNP, nonECRSwNP, and CTRL. IL5, IL1RL1, and IL1RAP were found to exhibit a significant positive correlation with ALOX15. Level of Evidence Level 3.

Applicability of Sniffin' Sticks Identification Test as a Screening Tool for Olfactory Dysfunction in Northeast China.

BACKGROUND Because most case of smell loss are unrecognized, a valid and reliable screening test for olfactory function is needed. The Sniffin' Sticks test is one of the most widely used olfactory tests. As olfaction can be affected by environment and social background, we investigated the regional applicability of Sniffin' Sticks identification subtest as a screening tool. MATERIAL AND METHODS Normosmic volunteers were recruited between May 2021 and August 2021. We collected data on participants' age, sex, and educational level. The Self-Reported Mini-Olfactory Questionnaire and identification test of Sniffin' Sticks test battery were used to assess their olfactory function. RESULTS A total of 688 subjects (316 male, 371 female) volunteered for the screening test. The mean age of participants was 30±7.69 years (range, 15-63 years), and the average score of all subjects was 12.7±0.81 points. The 3 least recognized items among all 16 tests were lemon (correct identification rate 5.4%), clove (correct identification rate 1.5%), and apple (correct identification rate 0.7%). For Self-Reported Mini-Olfactory Questionnaire, 48 of the 687 subjects (7%) stated that they could not recognize the smell of freshly mowed grass. CONCLUSIONS We investigated the applicability of using Sniffin' Sticks Identification test and Self-MOQ as a screening tool for olfactory dysfunction in northeast China. Most of the subjects enrolled in this study failed to reach the normative standard for their age groups in the Sniffin' Sticks test. We suggest the deletion or replacement of items with extremely low correct identification rates and that physicians who use the Sniffin's Sticks test in clinical practice test the applicability in advance to avoid misdiagnosis.

Immunoglobulin G4-related disease presenting with hypertrophy and sclerosis of the inferior turbinate.

Immunoglobulin G4-related disease (IgG4-RD) is a novel clinical disease entity characterized by elevated serum IgG4 concentration and tumefaction or tissue infiltration by IgG4+ plasma cells.1 We report the case of a 56-year-old man who presented with nasal obstruction for 5 years. Rhinoscopy revealed hypertrophy and sclerosis of the inferior turbinate, whereas computed tomography revealed inflammation of the anterior ethmoid sinus and frontal sinuses. An endoscopic inferior turbinectomy was performed, and IgG4-RD was definitively diagnosed based on the histopathological features of the turbinate tissue. Prednisolone was administered postoperatively. IgG4-RD presenting with hypertrophy and sclerosis of the inferior turbinate is rare. Awareness of IgG4-RD originating in the sinonasal cavity is essential to avoid delayed diagnosis.

Transcriptome analysis of long non-coding RNAs reveals NR_015556 lncRNA is a novel regulator for adipocyte differentiation.

Long non-coding RNAs (lncRNAs) have gained extensive attentions due to their significant roles in diverse biological process. However, the potential functions of lncRNAs participation in adipocyte differentiation have not been fully explored. In the present study, we globally profiled lncRNA expression using lncRNA microarray and identified 1745 lncRNA probes with differential expression on day 0 and day 4 post-induction in both C3H10T1/2 mesenchymal stem cells and 3T3-L1 preadipocytes. Furthermore, we showed that stable shRNA knockdown (KD) of NR_015556, a novel lncRNA that was significantly down-regulated in adipocyte differentiation, promoted adipocyte differentiation by increasing the number of lipid droplets and adipocyte markers such as Fabp4, Adipsin and Fasn. Mechanistically, NR_015556 KD attenuated the expression of Wnt signaling components Wnt10b and non-phospho (active) ß-catenin, and elevated adipocyte master factors Ppar-γ and C/EBPα levels. Conversely, pharmacological activation of Wnt10b-ß-catenin signaling by LiCl suppressed NR_015556 KD-induced enhancement of adipocyte differentiation and Ppar-γ and C/EBPα expression levels. Taken together, these results indicate that down-regulation of NR_015556 promotes adipocyte differentiation through inhibiting Wnt10b-ß-catenin signaling pathway and then elevating Ppar-γ and C/EBPα triggered transcriptional cascades.

[Analysis of allergen distribution and clinical characteristics of autumn allergic rhinitis in Changchun and surrounding areas].

Objective:To investigate the allergen characteristics, allergen distribution and clinical symptoms of autumn allergic rhinitis in Changchun and surrounding areas. Methods:The allergen test results of 1080 allergic rhinitis（AR） suspected patients from Changchun and surrounding areas were collected, from August to October 2019 and August to October 2020 in the Department of Otorhinolaryngology Head and Neck Surgery, the Second Hospital of Jilin University. The positive rates of major allergens and their differences in gender, age, different years and clinical symptom were compared and analyzed. Results:①Among the 1080 suspected AR patients, 804 patients（74.44%） had positive allergens. ②The top 3 allergens of autumn AR in Changchun and surrounding areas were Artemisia（36.20%）, Dwarf ragweed（33.24%） and Candida/Penicillium notarum/Cladosporium/Alternaria/Aspergillus niger（19.81%）. The positive rates of Artemisia and Dwarf ragweed were higher in men than in women（P<0.05）. ③Artemisia was the major allergen of autumn AR in juvenile group, youth group and middle-aged group. ④The positive rate of two or more allergens was 2.39 times that of single allergen. ⑤Patients with positive autumn pollen allergens had more severe symptoms of nasal congestion, red eye/eye itching and epiphora than those in other groups. Conclusion:Seasonal AR had typical clinical symptom characteristics. Major allergens in autumn AR in Changchun and surrounding areas are autumn pollen allergens（Artemisia, Dwarf ragweed, Humulus）. The distribution of those allergens was different in gender, age, and different years.

A Novel Long Noncoding RNA, Lnc-OAD, Is Required for Bone Morphogenetic Protein 2- (BMP-2-) Induced Osteoblast Differentiation.

Long noncoding RNAs (lncRNAs) play very important roles in cell differentiation. Our recent study has demonstrated that a novel lncRNA named lnc-OAD modulated 3T3-L1 adipocyte differentiation. In the present study, we examined the roles of lnc-OAD in bone morphogenetic protein 2- (BMP-2-) induced osteoblast differentiation. Lnc-OAD expression was increased during BMP-2-induced osteoblast differentiation in C3H10T1/2 mesenchymal stem cells and MC3T3-E1 preosteoblast cells. Knockdown of lnc-OAD expression by specific siRNA remarkably decreased early osteoblast differentiation. In addition, stable knockdown of lnc-OAD by lentivirus vector also significantly inhibited late osteoblast differentiation and matrix mineralization in vitro. Conversely, stably overexpressed lnc-OAD with lentiviral vector accelerated osteoblast differentiation. Mechanistically, knockdown of lnc-OAD reduced significantly the phosphorylation of AKT and the expression of Osterix induced by BMP-2, while overexpression of lnc-OAD enhanced the phosphorylation of AKT and the expression of Osterix. Taken together, our study suggests that lnc-OAD plays an important role in modulating BMP-2-induced osteoblast differentiation via, at least in part, regulating the AKT-Osterix signaling axis.

Role of PI3-Kinase in Angiotensin II-Induced Cardiac Hypertrophy: Class I Versus Class III.

Cardiac hypertrophy is an adaptive response to cardiac overload initially but turns into a decompensated condition chronically, leading to heart failure and sudden cardiac death. The molecular mechanisms involved in cardiac hypertrophy and the signaling pathways that contribute to the switch from compensation to decompensation are not fully clear. The aim of the current study was to examine the role of PI3-kinases Class I (PI3KC1) and Class III (PI3KC3) in angiotensin (Ang) II-induced cardiac hypertrophy. The results demonstrate that treatment of cardiomyocytes with Ang II caused dose-dependent increases in autophagy, with an increasing phase followed by a decreasing phase. Ang II-induced autophagic increases were potentiated by inhibition of PI3KC1 with LY294002, but were impaired by inhibition of PI3KC3 with 3-methyladenine (3-MA). In addition, blockade of PI3KC1 significantly attenuated Ang II-induced ROS production and cardiomyocyte hypertrophy. In contrast, blockade of PI3KC3 potentiated Ang II-induced ROS production and cardiac hypertrophy. Moreover, blockade of PI3KC1 by overexpression of dominant negative p85 subunit of PI3KC1 significantly attenuated Ang II-induced cardiac hypertrophy in normotensive rats. Taken together, these results demonstrate that both PI3KC1 and PI3KC3 are involved in Ang II-induced cardiac hypertrophy by different mechanisms. Activation of PI3KC1 impairs autophagy activity, leading to accumulation of mitochondrial ROS, and, hence, cardiac hypertrophy. In contrast, activation of PI3KC3 improves autophagy activity, thereby reducing mitochondrial ROS and leads to a protective effect on Ang II-induced cardiac hypertrophy.

Author Correction: CCT α is a novel biomarker for diagnosis of laryngeal squamous cell cancer.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

MicroRNA-761 suppresses remodeling of nasal mucosa and epithelial-mesenchymal transition in mice with chronic rhinosinusitis through LCN2.

BACKGROUND: Chronic rhinosinusitis (CRS) is characterized by persistent symptomatic inflammation of the nasal passage and sinus mucosa. Various microRNAs (miRs) have been implicated in CRS. Hence, the current study was conducted to explore the effect of microRNA-761 (miR-761) on remodeling of nasal mucosa and epithelial-mesenchymal transition (EMT). METHODS: Bioinformatics analysis was initially performed to predict the differentially expressed genes (DEGs) associated with CRS. Gene targeting relationship between miR-761 and lipocalin 2 (LCN2) was analyzed by bioinformatics analysis and verified using dual-luciferase reporter gene assay. Histopathological analyses of the nasal mucosa tissues were conducted via hematoxylin-eosin (HE) and alcian blue (AB)-periodic acid Schiff (PAS) staining. ELISA was employed to determine the IL-8 and MMP-9 levels. To define downstream pathway of miR-761, levels of proteins related to LCN2/Twist1 signaling pathway were assessed. Additionally, the effects of miR-761 on EMT, proliferation, and apoptosis were determined. RESULTS: LCN2 was highly expressed in CRS. LCN2 was a target of miR-761. miR-761 overexpression or LCN2 silencing decreased IL-8 and MMP-9 levels and morphological changes in nasal epithelial tissue from CRS mice. Overexpressed miR-761 or silenced LCN2 decreased the expression of LCN2 and Twist1, indicating LCN2/Twist1 signaling pathway was inactivated. Moreover, miR-761 overexpression or LCN2 silencing reduced the expression of N-cadherin and vimentin, while increased that of E-cadherin, suggesting inhibition of EMT. Furthermore, miR-761 overexpression or LCN2 silencing promoted cell proliferation and inhibited cell apoptosis in CRS. CONCLUSION: Taken together, miR-761 suppressed the remodeling of nasal mucosa through inhibition of LCN2 and the LCN2/Twist1 signaling pathway.

Identification of Susceptibility Genes to Allergic Rhinitis by Gene Expression Data Sets.

As an extremely prevalent disease worldwide, allergic rhinitis (AR) is a condition characterized by chronic inflammation of the nasal mucosa. To identify the finer molecular mechanisms associated with the AR susceptibility genes, differentially expressed genes (DEGs) in AR were investigated. The DEG expression and clinical data of the GSE19187 data set were used for weighted gene co-expression network analysis (WGCNA). After the modules related to AR had been screened, the genes in the module were extracted for Gene Ontology and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis, whereby the genes enriched in the KEGG pathway were regarded as the pathway-genes. The DEGs in patients with AR were subsequently screened out from GSE19187, and the sensitive genes were identified in GSE18574 in connection with the allergen challenge. Two kinds of genes were compared with the pathway-genes in order to screen the AR susceptibility genes. Receiver operating characteristic (ROC) curve was plotted to evaluate the capability of the susceptibility genes to distinguish the AR state. Based on the WGCNA in the GSE19187 data set, 10 co-expression network modules were identified. The correlation analyses revealed that the yellow module was positively correlated with the disease state of AR. A total of 89 genes were found to be involved in the enrichment of the yellow module pathway. Four genes (CST1, SH2D1B, DPP4, and SLC5A5) were upregulated in AR and sensitive to allergen challenge, whose potentials were further confirmed by ROC curve. Taken together, CST1, SH2D1B, DPP4, and SLC5A5 are susceptibility genes to AR.

Efficacy of posterior nasal neurectomy for allergic rhinitis combined with chronic rhinosinusitis with nasal polyps.

Background: Allergic rhinitis combined with chronic rhinosinusitis with nasal polyps (ARwCRSwNP) is very common clinically. Conventionally, the treatment for these patients is surgical method for CRSwNP followed by treatment with a nasal steroid spray or other antiallergic drugs to control AR. In recent years, some rhinologists introduced vidian neurectomy (VN) or posterior nasal neurectomy (PNN) into endoscopy to treat refractory AR and reported an encouraging outcome. Furthermore, we explore the control of recurrence of nasal polyps and improvement in symptoms after endoscopic PNN for the treatment of ARwCRSwNP. Objective: To investigate the control of recurrence of nasal polyps and improvement in symptoms after endoscopic PNN for the treatment of ARwCRSwNP. Methods: Eighty-five patients with ARwCRSwNP who were admitted to our hospital from November 2016 to July 2018 were enrolled in two groups. Group A underwent conventional functional endoscopic sinusitis surgery (FESS) combined with PNN; group B underwent conventional FESS alone. VAS, RQLQ, SNOT-22 and postoperative nasal endoscopy were used to evaluate the improvement in symptoms and the recurrence of nasal polyps. Results: The experimental group had better control of sneezing (p < .05) and rhinorrhea (p < .01) than the control group. For those who underwent surgery more than 6 months prior in both groups, the recurrence rate was 29.6% (8/27) in the experimental group and 44.4% (8/18) in the control group, and there was no significant difference (χ2 = .483, p = .487). Conclusion: FESS combined with PNN can improve the symptoms of sneezing and rhinorrhea caused by ARwCRSwNP more obviously than FESS alone, but there is no clear statistical advantage of this procedure for improving the overall symptoms and controlling the recurrence of nasal polyps.

CCT α is a novel biomarker for diagnosis of laryngeal squamous cell cancer.

Choline phosphate-based delivery systems can target the acidic tumor microenvironment. In this study, we set out to evaluate the diagnostic value of Choline phosphate cytidylyltransferase-α (CCTα) in laryngeal squamous cell cancer (LSCC). The expression of CCTα was detected using immunohistochemistry in 50 LSCC patients' tissues and 16 vocal polyps as control group. Then, clinical data was collected and we used receiver operating characteristic curve (ROC) to estimate the potential of CCTα as diagnostic biomarker. We found CCTα levels to be significantly high in the tissues derived from LSCC patients, (p < 0.001). Further, we observed a positive correlation of CCTα with tumor size (p < 0.001), TNM stage (p < 0.001), lymph node metastasis (p < 0.001) as well as the grade of LSCC malignancy (p < 0.001). Furthermore, AUC was determined to be 0.939 by ROC, and the optimal cutoff value 3.100, with 76.0% sensitivity and 100% specificity. We also found an epigenetic basis of CCTα over-expression in LSCC tissues with significantly reduced methylation of CCTα in LSCC tissues, compared to vocal polyps (p < 0.001). These results support epigenetically-induced over-expression of CCTα as a potential diagnostic marker for LSCC.

Identification of Pyrvinium, an Anthelmintic Drug, as a Novel Anti-Adipogenic Compound Based on the Gene Expression Microarray and Connectivity Map.

Obesity is a serious health problem, while the current anti-obesity drugs are not very effective. The Connectivity Map (C-Map), an in-silico drug screening approach based on gene expression profiles, has recently been indicated as a promising strategy for drug repositioning. In this study, we performed mRNA expression profile analysis using microarray technology and identified 435 differentially expressed genes (DEG) during adipogenesis in both C3H10T1/2 and 3T3-L1 cells. Then, DEG signature was uploaded into C-Map, and using pattern-matching methods we discovered that pyrvinium, a classical anthelminthic, is a novel anti-adipogenic differentiation agent. Pyrvinium suppressed adipogenic differentiation in a dose-dependent manner, as evidenced by Oil Red O staining and the mRNA levels of adipogenic markers. Furthermore, we identified that the inhibitory effect of pyrvinium was resulted primarily from the early stage of adipogenesis. Molecular studies showed that pyrvinium downregulated the expression of key transcription factors C/EBPa and PPARγ. The mRNA levels of notch target genes Hes1 and Hey1 were obviously reduced after pyrvinium treatment. Taken together, this study identified many differentially expressed genes involved in adipogenesis and demonstrated for the first time that pyrvinium is a novel anti-adipogenic compound for obesity therapy. Meanwhile, we provided a new strategy to explore potential anti-obesity drugs.

Desmoglein 3 Silencing Inhibits Inflammation and Goblet Cell Mucin Secretion in a Mouse Model of Chronic Rhinosinusitis via Disruption of the Wnt/ß-Catenin Signaling Pathway.

Chronic rhinosinusitis (CRS) is a common disease characterized by inflammation of the nose and paranasal sinuses lasting over 12 weeks. This study aims to evaluate the effect of desmoglein 3 (DSG3) on inflammatory response and goblet cell mucin secretion in a mouse model of CRS. The CRS-related differentially expressed genes and disease genes were screened using microarray-based gene expression analysis. Subsequently, CRS mouse models were established. The levels of pro-inflammatory factors TNF-α, IL-6, and IL-8 were measured by ELISA. In addition, loss-of-function experiment was conducted using siRNAs targeting DSG3 and ß-catenin. The secretion of mucins MUC5B and MUC5AC in goblet cells was detected, and the apoptosis of goblet cells was assessed. The regulatory effect of DSG3 on the Wnt/ß-catenin signaling pathway was analyzed by determining the mRNA and protein levels of DSG3, Wnt, ß-catenin, and GSK3ß. DSG3 was identified to be an upregulated gene in CRS, which was further documented in CRS mice models. Elevated inflammation and mucin production were noted in CRS mice models. Also, it was found that DSG3 or ß-catenin silencing could decrease the levels of TNF-α, IL-6, and IL-8, and the positive rates of MUC5B and MUC5AC while enhancing goblet cell apoptosis. The Wnt/ß-catenin signaling pathway was blocked by DSG3, evidenced by downregulated Wnt and ß-catenin as well as upregulated GSK3ß mRNA and protein levels. Overall, this study provides evidence that silencing DSG3 could inhibit the activation of the Wnt/ß-catenin signaling pathway, thus alleviating CRS.

Epigenetic changes: An emerging potential pharmacological target in allergic rhinitis.

The importance of epigenetics has increased due to identification of its role in the pathophysiology of a number of diseases including allergic rhinitis. Amongst the different epigenetic changes in allergic retinitis, deacetylation of histone proteins by histone deacetylase (HDACs), hypermethylation of DNA by DNA methyltransferases (DNMT) and alteration in post-transcriptional process by the changes in the levels of miRNA are widely studied. Studies conducted related to allergic rhinitis have shown the elevation in the levels of HDAC1, 3 and 11 in the nasal epithelia and HDAC inhibitors have shown effectiveness in decreasing the symptoms of rhinitis. Their beneficial effects are attributed to restoration of the expression of TWIK-related potassium channel-1, correction of cytokine profile along with normalization of Th1/Th2 imbalance. Another epigenetic change due to increase in DNMT activity may induce DNA hypermethylation in CpG sites in the airway epithelial cells and CD4+ T-cells. The reduction in DNA methylation decreases allergic symptoms and normalizes the over-reactive immune system. Mechanistically, allergens may promote the hypermethylation in the promoter region of IFN-γ gene in CD4+ T cells via activation of ERK pathway to decrease the expression of IFN-γ. In allergic rhinitis patients, there is also a downregulation of certain miRNAs including miR-135a, miR-146a, miR-181a, miR-155 and upregulation of miRNA19a. This review discusses the studies describing the epigenetic changes taking place in the host cells in response to allergen along with possible mechanisms.

Long non-coding RNA lnc-OAD is required for adipocyte differentiation in 3T3-L1 preadipocytes.

Long non-coding RNAs (lncRNAs) have gained extensive attentions due to their significant roles in diverse biological process. However, the potential functions of lncRNAs participation in adipocyte differentiation have not been fully explored. Here we identified a long non-coding RNA called lnc-OAD (lncRNA associated with osteoblast and adipocyte differentiation, transcribed from 1700018A04Rik gene), which modulated 3T3-L1 adipocyte differentiation. Lnc-OAD was up-regulated expression during 3T3-L1 differentiation and stable knockdown of lnc-OAD inhibited adipocyte differentiation in 3T3-L1 cells. Further mechanisms study revealed that silencing of lnc-OAD strongly elevated the protein expression of ß-catenin, and then decreased expression of adipocyte master transcription factors PPAR-γ and C/EBPα. The addition of IWR-1 up-regulated the expression of PPAR-γ and C/EBPα and rescued the impairment of adipocyte differentiation caused by lnc-OAD knockdown. Meanwhile, we also found mitotic clonal expansion (MCE) during the early stage of adipocyte differentiation was inhibited in lnc-OAD-knockdown cells. Taken together, our study reveals a novel function of lnc-OAD in modulating adipogenesis via influencing mitotic clonal expansion and regulating WNT/ß-catenin signaling pathway.

Modified endoscopic inferior meatal fenestration with mucosal flap for maxillary sinus diseases.

INTRODUCTION: This is a novel minimally invasive surgical method for maxillary sinus mucoceles and antrochoanal polyps. AIM: To describe a modified technique of inferior meatal fenestration with a mucosal flap for maxillary sinus diseases and to present a case series of subjects who underwent this procedure. The novel surgical technique and indications for this approach are also discussed. MATERIAL AND METHODS: The authors analyzed data from 32 cases involving patients who underwent resection of maxillary sinus mucoceles and antrochoanal polyps via modified endoscopic inferior meatal fenestration with a mucosal flap in the period from January, 2011 to January, 2016. The group included 19 men and 13 women, and the patients' mean age was 36.2 years (range: 11-56 years). Preoperative and postoperative imaging studies were available in all cases and were reviewed. RESULTS: Thirty-two cases are included in this study. The appearance of nasal and (or) maxillary sinus mucosa was observed in the follow-up at 1 month, 3 months and 6 months using endoscopes. Postoperative computed tomography was performed for only 9 patients in this study. The mean follow-up period was 56 (range: 10-82) months in these cases. All patients had an uneventful post-operative period. Postoperative symptoms were relieved gradually for 1 to 2 weeks after the operation. No patients experienced recurrent symptoms related to the mucocele. Mucocele and polyps recurrence was not observed. No patient showed re-stenosis and obstruction of the nasal cavity, facial pain or numbness during follow-up. CONCLUSIONS: Maxillary sinus mucoceles and antrochoanal polyps are completely excised via modified endoscopic inferior meatal fenestration with a mucosal flap. It could keep the nasal lateral wall intact.

Clinicopathologic and prognostic significance of VEGF, JAK2 and STAT3 in patients with nasopharyngeal carcinoma.

BACKGROUND: The aim of the study was to investigate the effect associated with the protein expression of VEGF, JAK2 and STAT3 on the clinicopathologic characteristics and prognosis in the development and progression of nasopharyngeal carcinoma (NPC). METHODS: Fifty NPC patients in addition to 20 patients with chronic nasopharyngitis (CNP) were recruited for the purposes of the study. Western blotting and immunohistochemistry methods were employed to evaluate the protein expressions of JAK2, STAT3 and VEGF in the NPC and CNP tissues, with their respective correlations with the clinicopathologic characteristics of NPC patients subsequently analyzed. Spearman's rank correlation coefficient and Kaplan-Meier method were conducted to evaluate the respective correlations of JAK2, STAT3 and VEGF with NPC as well as the survival rates of patients with NPC. Cox regression analyses was performed in determine the prognostic NPC factors. RESULTS: Compared with the CNP tissues, the NPC tissues exhibited elevated levels of JAK2, STAT3 and VEGF which were subsequently determined to share a positive correlation with T stages, lymph node metastasis (LNM), N stages and clinical stages, while a negative correlation with survival rates were observed in the NPC patients. Positive correlations between the expressions of JAK2, STAT3 and VEGF were detected among the NPC tissues. NPC patients survival time with negative expressions of JAK2, STAT3 and VEGF were observed to be longer than that of NPC patients with positive expressions of JAK2, STAT3 and VEGF. T stage, LNM, N stage, clinical stage. The expressions of JAK2, STAT3 and VEGF were discovered to be independent risk factors associated with the prognosis of patients with NPC. CONCLUSION: The results obtained from the present study support the notion that higher expressions of JAK2, STAT3 and VEGF may be correlated with the clinicopathologic characteristics and prognosis of patients suffering from NPC.

MicroRNA-185 inhibits cell proliferation while promoting apoptosis and autophagy through negative regulation of TGF-ß1/mTOR axis and HOXC6 in nasopharyngeal carcinoma.

OBJECTIVE: Accumulating studies have revealed that microRNAs (miRs) play a critical role in the development and progression of nasopharyngeal carcinoma (NPC), which is a disease with a remarkable racial and geographical distribution. In our study, through the alteration in the expression of microRNA-185 (miR-185) in NPC cells by microarray-based gene expression profiling, we subsequently evaluated its ability to influence NPC cells and associated mechanism. METHODS: The expressions of miR-185 and HOXC6 in NPC and paracancerous tissues collected from patients with NPC were detected. The CNE-2 cells with the lowest miR-185 among the five NPC cell lines (CNE-1, CNE-2, HNE-1, HNE-2, and 5-8F) were selected and transfected with a series of mimic or inhibitor of miR-185, or shRNA-against HOXC6. The Kaplan-Meier method was used to analyze the survival of patients. Besides, the reverse transcription quantitative polymerase chain reaction (RT-qPCR) and western blot analysis were used to determine the levels of related genes/proteins. By means of cell counting kit-8 (CCK-8) assay, transwell assay, flow cytometry, and AO staining, the influences miR-185 has on the processes associated with NPC, including cell proliferation, invasion, apoptosis and autophagy were evaluated. RESULTS: NPC was observed to decrease miR-185 but increase HOXC6. Dual luciferase reporter gene assay demonstrated that HOXC6 is a target gene of miR-185. Increased mRNA and protein levels of Bax, caspase-3, LC3 and Beclin1 and reduced levels of HOXC6, TGF-ß1, mTOR, Cyclin D1, PCNA, Bcl-2 were found by overexpression of miR-185. High expression of miR-185 and low expression of HOXC6 had longer survival time of NPC patients. Overexpressed miR-185 enhanced cell apoptosis and autophagy, and reduced cell proliferation and invasion, while miR-185 inhibitor was observed to have induced effects on the CNE-2 cells. CONCLUSION: Overall, the data show that miR-185 could negatively target HOXC6 to suppress cell proliferation, promotes apoptosis and autophagy through inhibiting TGF-ß1/mTOR axis in NPC. Thus, miR-185 is useful strategy for the treatment of NPC.