Roles of noncoding RNA in allergic rhinitis.

BACKGROUND: Allergic rhinitis (AR) is one of the most common respiratory noninfectious diseases and chronic inflammatory diseases, the incidence of which has been increasing in recent years. The main pathological characteristics of AR are repeated inflammation, airway hyperreactivity, mucus hypersecretion, and reversible airway obstruction due to inflammatory cell response. AR occurrence is associated with various factors, including those of genetic and environmental origins. Noncoding RNAs (ncRNAs) are a group of RNA molecules that cannot be converted into polypeptides. The three main categories of ncRNAs include microRNAs (miRNAs), long ncRNAs (lncRNAs), and circular RNAs (circRNAs). NcRNAs play a crucial role in controlling gene expression and contribute to the development of numerous human diseases. METHODS: Articles are selected based on Pubmed's literature review and the author's personal knowledge. The largest and highest quality studies were included. The search selection is not standardized. Several recent studies have indicated the relationship of ncRNAs with the development of respiratory allergic diseases. NcRNAs, including miRNAs, lncRNAs, and circRNAs, are important gene expression regulatory factors. We review the expression and function of ncRNAs in AR, their role as disease biomarkers, and their prospective applicability in future research and clinically. We also discuss interactions between ncRNAs and their influence on AR comprehensively, these interactions are essential for determining the underlying pathological mechanisms further and discovering new drug therapeutic targets. RESULTS: NcRNAs can be used as biomarkers for early AR diagnosis, disease surveillance and prognosis assessment. Various categories of ncRNAs play distinct yet interconnected roles and actively contribute to intricate gene regulatory networks. They are also therapeutic targets and biomarkers in other allergic diseases. CONCLUSION: This article demonstrates ncRNAs have a wide range of applications in AR treatment. The database covers three key areas: miRNAs, lncRNAs, and circRNAs. Additionally, potential avenues for future research to facilitate the practical application of ncRNAs as therapeutic targets and biomarkers will be explore. With further research and technological development, ncRNAs may provide additional innovative, effective solutions for AR treatment.

The relationship between imaging-based body composition abnormalities and long-term mortality in patients with liver cirrhosis.

BACKGROUND: Emerging evidence on cirrhosis suggests a close correlation between abnormality in body composition characteristics and poor prognosis. This study aimed to evaluate the impact of dynamic changes in body composition on the prognostic outcomes in patients with cirrhosis. METHODS: This retrospective analysis included 158 patients diagnosed as cirrhosis from January 2018 to August 2023. Skeletal muscle mass, muscle quality, visceral and subcutaneous adiposity were evaluated using computed tomography (CT) imaging at the third lumbar vertebra level. Competing risk model was performed four different body composition status (i.e., normal, only sarcopenia, only myosteatosis, and combined status) for liver-related mortality. We also explored the relationship between the dynamic change in body composition and long-term prognosis by applying Gray's test. RESULTS: Of the 158 cirrhotic patients (mean [SD] age, 57.1 [12.6] years), sarcopenia was present in 85 (60.1 %) patients, while 22 (13.9 %) patients had sarcopenic obesity and 68 (43.0 %) had myosteatosis. Patients solely diagnosed with sarcopenia exhibited a higher mortality rate compared to those with normal body composition (Gray's test, P=0.006), while patients solely diagnosed with myosteatosis or with a combination of sarcopenia and myosteatosis did not reach statistical significance (Gray's test, P=0.076; P=0.140). Multivariable analysis also revealed that VSR (HR=1.10 [1.01∼1.20]; P=0.028), sarcopenia (HR=2.73 [1.20∼6.22], P=0.017) and myosteatosis (HR=2.39 [1.10∼5.18], P=0.028) were significant independent predictors of liver-related deaths. Otherwise, patients exhibiting aggravating body composition during follow-up period were associated with a significantly higher mortality risk compared to those with normal or remission body composition status (HR=7.63 [1.12∼51.14]; P=0.036). CONCLUSION: Progressive alterations in body composition status appears to be associated with liver-related mortality in individuals with liver cirrhosis. Focusing on the management of skeletal muscle, along with visceral and subcutaneous adiposity, may contribute to improving the prognosis of cirrhotic patients.

Muscle mass dynamics is independently associated with long-term liver-related mortality in patients with cirrhosis.

Objectives: Sarcopenia has a detrimental impact on the prognosis of individuals with liver cirrhosis, however, the clinical significance of alterations in muscle mass remains uncertain. This study aims to investigate the influence of loss of skeletal muscle mass (LSMM) on the prognostic outcomes among patients diagnosed with cirrhosis. Methods: In this retrospective analysis, a total of 158 individuals with cirrhosis who visited our hospital during the period from January 2018 to August 2023 were included. Computed tomography was utilized to measure the cross-sectional area of the skeletal muscles at the level of the third lumbar vertebra. This measurement enabled the determination of the skeletal muscle index for the purpose of diagnosing sarcopenia. The annual relative change in skeletal muscle area (ΔSMA/y) was calculated for each patient, and LSMM was defined as ΔSMA/y < 0. To assess the risk factors associated with liver-related mortality, a competing risk model was applied. Results: Of the 158 cirrhotic patients, 95 (60.1 %) patients were identified as LSMM. The median of ΔSMA/y% was -0.9 (interquartile range [IQR], -3.8, 1.6) in all patients. Chronic kidney disease (CKD) was confirmed as a risk factor of LSMM. During a median follow-up period of 68.1 (IQR, 43.5, 105.0) months, 57 patients (36.1 %) died due to the liver-related diseases. The competing risk model found that LSMM was significantly associated with liver-related mortality in cirrhotic patients (hazard ratio [HR], 1.86; 95 % CI, 1.01-3.44, p = 0.047). Cumulative survival was significantly higher in patients without LSMM than in those with LSMM (p = 0.004). Survival rates at 1-, 3-, and 5-years were 96.8 %, 81.0 %, and 65.1 %, respectively, in patients without LSMM, and 97.9 %, 80.0 %, and 56.8 %, respectively, in patients with LSMM. Conclusion: The utilization of LSMM can be valuable in the prediction of liver-related mortality among individuals diagnosed with liver cirrhosis. Paying attention to the management of skeletal muscle might play a role in enhancing the prognosis of patients with cirrhosis. Clinical relevance statement: This study provides an additional indicator-LSMM for clinicians to help predict the liver-related mortality in patients diagnosed with cirrhosis.

Establishment of an in situ model to explore the tumor immune microenvironment in head and neck squamous cell carcinoma.

OBJECTIVE: Establish an in situ model for investigating HNSCC, focusing on tumor growth, metastasis, and the immune microenvironment. METHODS: Generated a monoclonal SCCVII-ZsGreen cell line through lentiviral transfection. Selected monoclonal lines with growth rates similar to the original SCCVII for in vivo tumorigenesis. Monitored tumor development and metastasis through fluorescence in vivo imaging. Employed immunohistochemistry to assess immune cell distribution in the tumor microenvironment. RESULTS: SCCVII-ZsGreen exhibited comparable proliferation and in vivo tumorigenicity to SCCVII. In situ tumor formation on day 10, with cervical metastasis in C57BL/6 mice by day 16. No significant fluorescence signals in organs like liver and lungs, while SCCVII-ZsGreen presence confirmed in cervical lymph node metastases. Immunohistochemistry revealed CD4+ T, CD8+ T, B, and dendritic cells distribution, with minimal macrophages. CONCLUSION: Our model is a valuable tool for studying HNSCC occurrence, metastasis, and immune microenvironment. It allows dynamic observation of tumor development, aids preclinical drug experiments, and facilitates exploration of the tumor immune contexture.

Anlotinib suppressed tumor cell proliferation and migration in hypopharyngeal carcinoma.

OBJECTIVE: The purpose of this study is to study the in-vitro effects of multitarget inhibitor anlotinib on hypopharyngeal cancer cell proliferation and cell migration, and the underlying mechanism, which will provide new drug choices for hypopharyngeal cancer treatment. METHODS: The Hypopharyngeal cancer Fadu cells were treated with anlotinib at a concentration of 0, 5, and 10 µmoL/L, respectively. Cell counting kit-8 and the colony-forming assay were used to detect the inhibition of cell proliferation. Wound-healing assay and transwell assay were used to detect the migration and invasion ability of cells. Flow cytometry was used to detect the effects of anlotinib on cell cycle and apoptosis. RT-qPCR and Western blot were used to measure gene expression levels. RESULTS: CCK-8 and colony-forming assay showed that anlotinib could significantly inhibit cell proliferative activity. Wound-healing assay and transwell assay showed that anlotinib could inhibit cell migration and scratch. These results showed that anlotinib has obvious antitumor activity. Flow cell cycle experiment showed that anlotinib could promote Fadu cell apoptosis and block the G2/M phase for inhibiting cell proliferation. In addition, anlotinib decreased the expression of HIF-1α. CONCLUSIONS: Anlotinib has an excellent suppressing effect on the proliferation, migration, and invasion of hypopharyngeal cancer Fadu cells in-vitro. Moreover, it can play an anti-tumor role through blocking cell cycle G2/M and promoting apoptosis, which may be related to the decrease of HIF-1a expression. Our study would provide a potential treatment method for patients with hypopharyngeal cancer. LEVEL OF EVIDENCE: Level 3.

Anlotinib suppressed tumor cell proliferation and migration in hypopharyngeal carcinoma

Abstract Objective The purpose of this study is to study the in-vitro effects of multitarget inhibitor anlotinib on hypopharyngeal cancer cell proliferation and cell migration, and the underlying mechanism, which will provide new drug choices for hypopharyngeal cancer treatment. Methods The Hypopharyngeal cancer Fadu cells were treated with anlotinib at a concentration of 0, 5, and 10 μmoL/L, respectively. Cell counting kit-8 and the colony-forming assay were used to detect the inhibition of cell proliferation. Wound-healing assay and transwell assay were used to detect the migration and invasion ability of cells. Flow cytometry was used to detect the effects of anlotinib on cell cycle and apoptosis. RT-qPCR and Western blot were used to measure gene expression levels. Results CCK-8 and colony-forming assay showed that anlotinib could significantly inhibit cell proliferative activity. Wound-healing assay and transwell assay showed that anlotinib could inhibit cell migration and scratch. These results showed that anlotinib has obvious antitumor activity. Flow cell cycle experiment showed that anlotinib could promote Fadu cell apoptosis and block the G2/M phase for inhibiting cell proliferation. In addition, anlotinib decreased the expression of HIF-1α. Conclusions Anlotinib has an excellent suppressing effect on the proliferation, migration, and invasion of hypopharyngeal cancer Fadu cells in-vitro. Moreover, it can play an anti-tumor role through blocking cell cycle G2/M and promoting apoptosis, which may be related to the decrease of HIF-1a expression. Our study would provide a potential treatment method for patients with hypopharyngeal cancer. Level of evidence: Level 3.

Long non-coding RNA FAM239A promotes tumor cell proliferation and migration by regulating tyrosine phosphatase Src homology 2 domain-containing phosphatase 2 in head and neck squamous cell carcinoma.

OBJECTIVE: Head and neck squamous cell carcinoma (HNSCC), is one of the malignant tumors with high recurrence and metastasis. The family with sequence similarity (FAM) of non-coding RNAs promoted tumorigenesis and metastasis. But so far, long non-coding RNA (lncRNA) FAM239A's function in HNSCC regulation remains unclear. This study aimed to explore the lncRNA FAM239A function and regulation mechanism in HNSCC cell proliferation and migration. DESIGN: The expression level of lncRNA FAM239A and tyrosine phosphatase Src homology 2 domain-containing phosphatase 2 (SHP2) in HNSCC tumor tissue was tested by quantitative polymerase chain reaction. The cell proliferation and migration were tested by cell counting kit 8, kinetic live cell assay, and wound healing assay. The differential expression of SHP2 and immune infiltration in HNSCC were analyzed in the tumor immune estimation response and human protein atlas databases. And the survival analysis of SHP2 in HNSCC was analyzed in the gene expression profiling interactive analysis 2 databases. The SHP2 expression was tested by western blotting when lncRNA FAM239A overexpression and knockdown. RESULTS: LncRNA FAM239A and SHP2 were ectopically expressed in HNSCC tumor tissue. Cell proliferation and wound healing assays showed that lncRNA FAM239A promoted tumor cell proliferation and migration. SHP2 was overexpressed in HNSCC tumor tissue by database analyses, and the higher SHP2 expression caused poorer overall survival and disease-free survival in HNSCC patients. SHP2 expression was positively regulated by lncRNA FAM239A. CONCLUSIONS: LncRNA FAM239A promoted HNSCC cell proliferation and migration through upregulating SHP2 expression, which potentially provided new regulators for HNSCC.

Death-associated protein 3 in cancer-discrepant roles of DAP3 in tumours and molecular mechanisms.

Cancer, ranks as the secondary cause of death, is a group of diseases that are characterized by uncontrolled tumor growth and distant metastasis, leading to increased mortality year-on-year. To date, targeted therapy to intercept the aberrant proliferation and invasion is crucial for clinical anticancer treatment, however, mutant expression of target genes often leads to drug resistance. Therefore, it is essential to identify more molecules that can be targeted to facilitate combined therapy. Previous studies showed that death associated protein 3 (DAP3) exerts a pivotal role in regulating apoptosis signaling of tumors, meanwhile, aberrant DAP3 expression is associated with the tumorigenesis and disease progression of various cancers. This review provides an overview of the molecule structure of DAP3 and the discrepant roles played by DAP3 in various types of tumors. Considering the molecular mechanism of DAP3-regulated cancer development, new potential treatment strategies might be developed in the future.