Background: Solute carrier family 6 member 8 (SLC6A8) is known to be involved in the development of human tumors; however, the effect of SLC6A8 on the growth of non-small cell lung cancer (NSCLC) remains unclear. Here, we explored the role and potential action mechanism of SLC6A8 in NSCLC. Methods: We used public databases [Oncomine, Gene Expression Omnibus (GEO), and The Cancer Genome Atlas (TCGA)] to explore the expression of SLC6A8 in NSCLC. Additionally, we used immunohistochemistry to detect the expression of SLC6A8 in NSCLC clinicopathological tissues (cancer and adjacent tissues) and Western blotting to detect the expression of SLC6A8 in NSCLC clinicopathological tissues, NSCLC cell lines (A549, H1299, H520, and H1975), and a normal epithelial cell line (BEAS-2B). Using overexpression and knockdown of the SLC6A8 gene, we analyzed the in vitro effects of SLC6A8 on the proliferation, invasion, and epithelial-mesenchymal transition (EMT) of NSCLC and also the possible molecular mechanism with Notch signaling pathway. Results: Bioinformatic analysis demonstrated that SLC6A8 is highly expressed in NSCLC and is related to poor prognosis. We found that the expression of the SLC6A8 protein in human lung cancer tissues was significantly higher than that in adjacent tissues. In addition, it was also significantly higher in lung cancer cell lines (A549, H1299, H520, and H1975) than that in normal lung epithelium-BEAS-2B. Moreover, SLC6A8 overexpression promotes the proliferation, migration and invasion in vitro in NSCLC, accompanied by the activation of notch signaling pathway and the up-regulation of MMP9 and E-cadherin proteins. Knocking down SLC6A8 can inhibit the above effects on cells. Conclusions: SLC6A8 promotes the malignant progression of NSCLC and activates the Notch signaling pathway. Therefore, SLC6A8 is expected to become a molecular target for NSCLC treatment.

Background: Aloin, as a bioactive compound, has a variety of pharmacological functions, but its effects on combined allergic rhinitis and asthma syndrome (CARAS) have not been studied. To clarify the protective effect and mechanism of aloin in the treatment of CARAS by network pharmacology, molecular dynamics simulation and experiment.Methods: The targets of aloin, allergic rhinitis and asthma were obtained from various databases. The protein interaction network was constructed for the common targets, and molecular docking and molecular dynamics simulations were performed for the core targets. Functional and pathway enrichment analysis of common targets was also performed using R software. Varieties of biological experiments were conducted to verify the effect of aloin on the inflammatory changes of CARAS and its regulatory mechanism.Results: A total of 42 anti-allergic rhinitis and 58 anti-asthma targets were obtained, and 5 core anti-allergic rhinitis and 6 core anti-asthma targets were identified using topological analysis. GO and KEGG analyses showed that endopeptidase activity and MAPK signaling pathway played important roles in allergic rhinitis and asthma. Molecular docking and molecular dynamics simulations showed that aloin could stably bind to the core target proteins. Experimental verification showed that aloin significantly inhibited the expression of inflammatory factors, and may regulate CARAS by down-regulating MAPK signaling related proteins.Conclusion: This study identified the protective effect, potential target and mechanism of aloin on CARAS. It provides reference for understanding the molecular mechanism and clinical application of aloin in the ameliorates of CARAS.

Background: The primary factor of cancer mortality is lung tumor. ABI3BP gene encodes an extracellular matrix bind protein associated to multiplication and derivation. However, the prognosis score of ABI3BP for lung tumor and its relation with immunity cellular infiltration for lung tumor have not been reported.Methods: Public repository systems (Timer, GEPIA, TCGA, HPA) were utilized to explore expression of ABI3BP for lung tumor, and explored the relation of ABI3BP and clinicopathological parameters. TCGA information set was utilized for cox analysis for data with one or more variables of ABI3BP for lung tumor. STRING was utilized to explore ABI3BP regulatory networks. GO/KEGG enrichment analysis as well as enrichment analysis of gene sets were carried out for ABI3BP co-expression via R package. And finally we explored the relation of expression of ABI3BP and lung tumor immunity invasion, exploring the influence of ABI3BP level of expression on immunotreatment and whether immunity invasion would affect the prognosis of patients with lung tumor.Results: ABI3BP is downregulated in LUAD and LUSC, and associated to lung tumor phase and prognosis. Univariate and multivariate cox regression showed that ABI3BP was an independent prognostic factor in patients with lung tumors. The extracellular matrix protein-coding gene and the ABI3BP-related gene were intersected to obtain 10 hub genes. On the basis of GO/KEGG enrichment analysis, hub genes are closely associated to immunity-associated pathways including T cell receptor signaling pathway, immune response−activating cell surface receptor signaling pathway. Finally, the expression of ABI3BP is closely related to immune cell infiltration and immune cell marker set, and the expression of ABI3BP can help predict the therapeutic effect of immune checkpoint inhibitors and improve the prognosis of patients.Conclusion: ABI3BP could be a new target for lung tumor that could be utilized as a diagnostic and therapeutic tool.

Details of patients hospitalized for asthma exacerbation in mainland China are lacking. To improve disease control and reduce economic burden, a large sample survey among this patient population is indispensable. This study aimed to investigate the clinical characteristics and outcomes of such patients. A retrospective study was conducted on patients hospitalized for asthma exacerbation in 29 hospitals of 29 regions in mainland China during the period 2013 to 2014. Demographic features, pre-admission conditions, exacerbation details, and outcomes were summarized. Risk factors for exacerbation severity were analyzed. There were 3,240 asthmatic patients included in this study (57.7% females, 42.3% males). Only 28.0% used daily controller medications; 1,287 (39.7%) patients were not currently on inhaled corticosteroids. Acute upper airway infection was the most common trigger of exacerbation (42.3%). Patients with severe to life-threatening exacerbation tended to have a longer disease course, a smoking history, and had comorbidities such as hypertension, chronic obstructive pulmonary disease (COPD), and food allergy. The multivariate analysis showed that smoking history, comorbidities of hypertension, COPD, and food allergy were independent risk factors for more severe exacerbation. The number of patients hospitalized for asthma exacerbation varied with seasons, peaking in March and September. Eight patients died during the study period (mortality 0.25%). Despite enhanced education on asthma self-management in China during recent years, few patients were using daily controller medications before the onset of their exacerbation, indicating that more educational efforts and considerations are needed. The findings of this study may improve our understanding of hospital admission for asthma exacerbation in mainland China and provide evidence for decision-making.

COL6A6 inhibits the proliferation and metastasis of non-small cell lung cancer through the JAK signalling pathway Han Qiao, Yan Feng, Huaping Tang