Diverse Endotypes of Chronic Rhinosinusitis and Clinical Implications.

Chronic rhinosinusitis (CRS) is a highly heterogeneous disease characterized by inflammation in the nasal and sinus mucosa. The CRS phenotypes, based on the presence or absence of nasal polyps, are known as CRS with nasal polyps (CRSwNP) and CRS without nasal polyps (CRSsNP). However, this classification has limitations in fully capturing the mechanisms and clinical manifestations of CRS. To address the heterogeneity of CRS, there has been a growing focus on classifying the condition into distinct endotypes. Endotype classification involves grouping patients based on specific molecular, immunological, and clinical characteristics, allowing for more personalized and targeted treatment approaches.This review delves into the current state of endotype classifications for CRS. It explores the role of geographic factors, microbiome, and subphenotype in shaping different endotypes. Additionally, the review examines how various clinical features are associated with specific endotypes, providing valuable insights into tailoring treatment options for better outcomes and transitions between different endotypes.Overall, this review offers a comprehensive and up-to-date perspective on the intricate realm of CRS endotype classifications. By unraveling the molecular and clinical intricacies, this review lays the foundation for more precise, effective, and individualized treatment strategies in the management of CRS.

IL-10 family cytokines in chronic rhinosinusitis with nasal polyps: From experiments to the clinic.

Chronic rhinosinusitis with nasal polyps (CRSwNP) is considered a nasal sinus inflammatory disease that can be dominated by immune cells and cytokines. IL-10 family cytokines exert essential functions in immune responses during infection and inflammation. Recently, the understanding of the roles of the IL-10 family in CRSwNP is being reconsidered. IL-10 family members are now considered complex cytokines that are capable of affecting epithelial function and involved in allergies and infections. Furthermore, the IL-10 family responds to glucocorticoid treatment, and there have been clinical trials of therapies manipulating these cytokines to remedy airway inflammatory diseases. Here, we summarize the recent progress in the understanding of IL-10 family cytokines in CRSwNP and suggest more specific strategies to exploit these cytokines for the effective treatment of CRSwNP.

MicroRNAs regulating mucin type O-glycan biosynthesis and transforming growth factor ß signaling pathways in nasal mucosa of patients with chronic rhinosinusitis with nasal polyps in Northern China.

BACKGROUND: Chronic rhinosinusitis with nasal polyps (CRSwNP) is a persistent sinonasal mucosa inflammatory disease. MicroRNAs (miRNAs) that are involved in the pathogenesis of CRSwNP in Northern China remain unknown. METHODS: A miRCURY™ LNA Array was used to analyze miRNA profiles in nasal mucosa tissues of CRSwNP patients (n = 19) and healthy controls (n = 10). Subsequent pathways were predicted by DIANA-mirPath software. RESULTS: Five upregulated miRNAs, including miR-210-5p, miR-3178, miR-585-3p, miR-3146, and miR-320e, and 19 downregulated miRNAs, including miR-32-3p, miR-1299, miR-3196, miR-3924, and miR-548e-3p, were differentially expressed (p < 0.05, fold change >2) in tissues of CRSwNP vs controls. Utilizing the Kyoto Encyclopedia of Genes and Genomes database (KEGG), which is an online database for pathway mapping, mucin type O-glycan biosynthesis pathway was significantly enriched in upregulated miRNAs. Transforming growth factor-beta (TGF-ß), transient receptor potential (TRP) channels, and the mitogen-activated protein kinase (MAPK) signaling pathway were significantly linked to downregulated miRNAs. CONCLUSION: The mucin type O-glycan biosynthesis pathway and TGF-ß signaling pathway are regulated by miRNAs, which could be our focus in the future studies.

Circular RNA: a novel biomarker for progressive laryngeal cancer.

Circular RNAs (circRNAs), a class of endogenous RNAs, are characterized by covalently closed continuous loop without 5' to 3' polarity and polyadenylated tail. Recent studies indicated that circRNAs might play an important role in cancer. However, the function of circRNA in laryngeal squamous cell cancer tissues (LSCC) is still unknown. In this study, we investigated the expression of circRNAs in 4 paired LSCC tissues and adjacent non-tumor tissues by microarray analysis. Results showed significant upregulation (n = 302) of or downregulation (n = 396) of 698 circRNAs in LSCC tissues. We further detected hsa_circRNA_100855 as the most upregulated circRNA and hsa_circRNA_104912 as the most downregulated circRNA using qRT-PCR methods. Results showed that hsa_circRNA_100855 level was significantly higher in LSCC than in the corresponding adjacent non-neoplastic tissues. Patients with T3-4 stage, neck nodal metastasis or advanced clinical stage had higher hsa_circRNA_100855 expression. The hsa_circRNA_104912 level was significantly lower in LSCC than in corresponding adjacent non-neoplastic tissues. Patients with T3-4 stage, neck nodal metastasis, poor differentiation or advanced clinical stage had a lower hsa_circRNA_104912 expression. Overall, our data suggest that circRNAs play an important role in the tumorigenesis of LSCC and may serve as novel and stable biomarkers for the diagnosis and progress of LSCC.

Long noncoding RNA NEAT1 promotes laryngeal squamous cell cancer through regulating miR-107/CDK6 pathway.

BACKGROUND: Long noncoding RNA nuclear paraspeckle assembly transcript 1 (NEAT1) plays key role in the progression of some human cancers. However, the role of NEAT1 in human laryngeal squamous cell cancer (LSCC) is still unknown. We therefore investigated the expression and function of NEAT1 in LSCC. METHODS: NEAT1 level in LSCC and adjacent non-neoplastic tissues were detected by qRT-PCR. NEAT1 was knockdown in LSCC cells and cell proliferation, apoptosis and cell cycle were examined. The growth of xenografts with NEAT1 knockdown LSCC cells was analyzed. RESULTS: NEAT1 level was significantly higher in LSCC than in corresponding adjacent non-neoplastic tissues, and patients with neck nodal metastasis or advanced clinical stage had higher NEAT1 expression. Moreover, siRNA mediated NEAT1 knockdown significantly inhibited the proliferation and induced apoptosis and cell cycle arrest at G1 phase in LSCC cells. The growth of LSCC xenografts was significantly suppressed by the injection of NEAT1 siRNA lentivirus. Furthermore, NEAT1 regulated CDK6 expression in LSCC cells which was mediated by miR-107. CONCLUSION: NEAT1 plays an oncogenic role in the tumorigenesis of LSCC and may serve as a potential target for therapeutic intervention.