Background Chronic obstructive pulmonary disease (COPD) is characterized by airway obstruction and progressive lung inflammation. As the primary ingredient of a traditional Chinese medical herb, Baicalin has been previously shown to possess anti-inflammatory abilities. Thus, the current study aimed to elucidate the mechanism by which baicalin alleviates COPD. Methods Baicalin was adopted to treat cigarette smoke in extract-exposed MLE-12 cells after which cell viability and apoptosis were determined. The production of tumor necrosis factor alpha (TNF-α), interleukin-6 (IL-6), IL-8 were determined by enzyme-linked immunoassay. A COPD mouse model was constructed via exposure to cigarette smoke and lipopolysaccharide, baicalin treatment. Lung function and inflammatory cell infiltration were determined and the production of Muc5AC, TNF-α, IL-6, IL-8 in the bronchoalveolar lavage fluid (BALF) was assayed by ELISA. The effect of HSP72 and JNK on COPD following treatment with baicalin was assessed both in vivo and in vitro by conducting loss- and gain- function experiments. Results Baicalin improved lung function evidenced by reduction in inflammatory cell infiltration and Muc5AC, TNF-α, IL-6 and IL-8 levels observed in BALF in mice. Baicalin was further observed to elevate cell viability while inhibited apoptosis and TNF-α, IL-6 and IL-8 levels in MLE-12 cells. Baicalin treatment increased HSP72 expression, while its depletion reversed the effect of baicalin on COPD. HSP72 inhibited the activation of JNK, while JNK activation was found to inhibit the effect of baicalin on COPD. Conclusions Baicalin upregulated the expression of HSP72, resulting in the inhibition of JNK signaling activation, which ultimately alleviates COPD.
Background Previous studies have reported that soluble fms‐like tyrosine kinase‐1 (sFlt‐1) possesses anti‐tumor effects by inhibiting angiogenesis in many cancers. Exosomes can be engineered as delivery vehicles for transferring functional biomolecules, such as proteins, lipids, and nucleic acids (DNA, mRNA, and miRNA) to target cells to affect inflammation, apoptosis, and angiogenesis. The purpose of this study was to investigate whether exosomes can function as efficient carriers of sFlt‐1 in vitro and in vivo, to play a role in SCLC therapy. Methods We adopted three different methods: TEM, NTA and western blot analysis to characterize the cell‐derived exosomes from NCI‐H69 SCLC cell line and normal bronchial epithelial BEAS‐2B cell line. we next explored the effects of these exosomes on HUVE cell proliferation and migration in vitro.To verify sFlt‐1‐loaded exosomes suppress the tumor growth in vivo,we established subcutaneous xenografts in nude mice using the NCI‐H69 cell line. Results We observed that NCI‐H69‐exo significantly increased human umbilical vein endothelial cells (HUVEC) migration compared to BEAS‐2B‐exo in vitro and in vivo. sFlt‐1 protein expression was statistically higher in BEAS‐2B‐exo than NCI‐H69‐exo. sFlt‐1 protein or sFlt‐1‐enriched exosomes can inhibit the migration of HUVECs. Furthermore, sFlt‐1‐enriched exosomes exhibited higher inhibition efficacy on pro‐angiogenesis of NCI‐H69‐exo in comparison with the same concentration of sFlt‐1 protein. Intriguingly, sFlt‐1‐loaded exosomes showed marked anti‐tumor activity by inhibiting the growth of NCI‐H69 tumor xenografts. CD31 staining revealed that sFlt‐1‐loaded exosomes significantly reduced the vascular density of experimental mice. sFlt‐1‐loaded exosomes markedly induced tumor apoptosis and inhibited tumor cell proliferation in mice. Conclusion Exosomes from a SCLC cell line contain low levels of sFlt‐1 and significantly increased the migration of HUVECs. SFlt‐1‐enriched exosomes can inhibit NCI‐H69‐exo‐induced HUVEC migration. Exosomes enriched in sFlt‐1 have the potential to be effective therapeutic agents for SCLC.
Background Circular RNAs (circRNAs) play vital roles in non‐small cell lung cancer (NSCLC) progression. Our research analyzed the role of circ_0110498 on the cisplatin (DDP) resistance of NSCLC. Methods Cell glycolysis was analyzed by measuring glucose consumption and lactate production. Protein expression was determined by western blot analysis. The expression of circ_0110498, microRNA (miR)‐1287‐5p and RBBP4 was detected by RT‐qPCR assay. Cell counting kit‐8, colony formation and transwell assays, together with flow cytometry were conducted to analyze cell DDP resistance, proliferation, metastasis and apoptosis. Results Circ_0110498 expression was elevated in DDP‐resistant NSCLC tissues and cells. Circ_0110498 silencing not only suppressed the DDP resistance of NSCLC cells by inhibiting cell growth, metastasis and glycolysis, but also enhanced the DDP sensitivity of NSCLC tumors. MiR‐1287‐5p was sponged by circ_0110498, and its inhibitor also reversed the effect of circ_0110498 silencing on the DDP resistance of NSCLC cells. MiR‐1287‐5p interacted with RBBP4, and RBBP4 overexpression partly reversed the inhibitory effect of miR‐1287‐5p on the DDP resistance of NSCLC cells. Conclusion Circ_0110498 facilitated DDP resistance partly through mediating the miR‐1287‐5p/RBBP4 signaling in NSCLC.
Objective. The purpose of the present study was to explore the biomarkers related to lung cancer based on the bioinformatics method, which might be new targets for lung cancer treatment. Methods. GSE17681 and GSE18842 were obtained from the Gene Expression Omnibus (GEO) database. The differentially expressed miRNAs (DEMs) and genes (DEGs) in lung cancer samples were screened via the GEO2R online tool. DEMs were submitted to the mirDIP website to predict target genes. Gene Ontology (GO) analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis were conducted via uploading DEGs to the DAVID database. The protein-protein interaction network (PPI) of the DEGs was analyzed by STRING’s online tool. Then, the PPI network was visualized using Cytoscape 3.8.0. Results. 46 DEMs were identified in GSE17681, and the website predicted that there were 873 target genes of these DEMs. 1029 DEGs were identified in the GSE18842 chip. GO analysis suggested that the co-DEGs participated in the canonical Wnt signaling pathway, regulation of the Wnt signaling pathway, a serine/threonine kinase signaling pathway, the Wnt signaling pathway, and cell-cell signaling by Wnt. KEGG analysis results showed the co-DEGs of GSE17681 and GSE18842 were related to the Hippo signaling pathway and adhesion molecules. In addition, six hub genes that were related to lung cancer were identified as hub genes, including mTOR, NF1, CHD7, ETS1, IL-6, and COL1A1. Conclusions. The present study identified six hub genes that were related to lung cancer, including mTOR, NF1, CHD7, ETS1, IL-6, and COL1A1, which might be a potential target for lung cancer.
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