Monitoring the infection behavior of avian influenza viruses is crucial for understanding viral pathogenesis and preventing its epidemics among people. A number of viral labeling methods have been utilized for tracking viral infection process, but most of them are laborious or decreasing viral activity. Herein we explored a lipid biosynthetic labeling strategy for dynamical tracking the infection of H5N1 pseudotype virus (H5N1p) in host. Biotinylated lipids (biotinyl Cap-PE) were successfully incorporated into viral envelope when it underwent budding process by taking advantage of host cell-derived lipid metabolism. Biotin-H5N1p virus was effectively in situ–labeled with streptavidin-modified near-infrared quantum dots (NIR SA-QDs) using streptavidin-biotin conjugation with well-preserved virus activities. Dual-labeled imaging obviously shows that H5N1p viruses are primarily taken up in host cells via clathrin-mediated endocytosis. In animal models, Virus-conjugated NIR QDs displayed extraordinary photoluminescence, superior stability, and tissue penetration in lung, allowing us to long-term monitor respiratory viral infection in a noninvasive manner. Importantly, the co-localization of viral hemagglutinin protein and QDs in infected lung further conformed the dynamic infection process of virus in vivo. Hence, this in situ QD-labeling strategy based on cell natural biosynthesis provides a brand-new and reliable tool for noninvasion visualizing viral infection in body in a real-time manner.
Background: The transcription factors (TFs)-miRNA-mRNA network plays an important role in a variety of diseases. The TFs-miRNA-mRNA network related to idiopathic pulmonary fibrosis (IPF) remains unclear.Methods: GSE110147 and GSE53845 datasets from GEO database were used to process differential gene (DEGs) analysis, GSEA, WGCNA, Gene ontology and KEGG analysis. GSE13316 dataset were used to perform differential miRNA (DEMs) analysis and TFs prediction. Finally, a TFs-miRNA-mRNA network related to IPF was constructed, and the function was performed by GO and KEGG analysis. And twenty TFs in the network were verified by qPCR.Results: Through our analysis, 53 DEMs and 3675 DEGs were screened. The GSEA results suggested these genes were mainly related to protein digestion and absorption. WGCNA results showed that these DEGs were divided into eight modules, and the GO and KEGG analysis results of turquoise module genes showed that these 69 turquoise module genes were mainly enriched in metabolism. Besides, a TFs-miRNA-mRNA network, including 35 TFs, 12 miRNAs and 84 mRNAs, was constructed. Ultimately, the functional enrichment analysis showed that the TFs-miRNA-mRNA network mainly related to microtubule pathway, apoptotic signaling pathway and PI3K-Akt signaling pathway. Furthermore, experimental verification for TFs showed ARNTL, TRIM28, EZH2, BCOR and ASXL1 were sufficiently up-regulated in TGF-β1 treatment groups, while BCL6, BHLHE40, FOXA1 and EGR1 were significantly down-regulated. Conclusions: The novel TFs-miRNA-mRNA network that we constructed could provide new insights into the underlying molecular mechanisms of IPF. ARNTL, TRIM28, EZH2, BCOR, ASXL1, BCL6, BHLHE40, FOXA1 and EGR1 may play important role in IPF and become effective biomarker for diagnosis and treatment.
Warburg effect plays a crucial role in bladder cancer (Bca) development. However, the mechanism by which glycolysis is involved in Bca remains poorly understood. CircRNAs commonly play a regulatory role in tumor progression. Our study discovered and identified a novel circRNA, hsa_circ_0000235 (circ235), and investigated its role in the glycolytic process, which further results in the progression of Bca. We applied qRT-PCR to assess its clinicopathological relevance and evaluated its proliferation, migration, and glycolytic capacity. We investigated its mechanism using RNA immunoprecipitation, dual-luciferase reporters, and fluorescence in situ hybridization. The findings demonstrated that circ235 was dramatically increased in Bca tissues and was related to a worse prognosis. In vitro studies revealed that circ235 accelerated the rate of extracellular acidification and promoted glucose uptake and lactate manufacture in Bca cells. Additionally, it strengthened the proliferative and migratory capacities. Experiments on animals revealed that downregulating circ235 dramatically reduced carcinogenesis and tumor growth. Circ235 activates monocarboxylate transporter 4 (MCT4) by sponging miR-330-5p, which promotes glycolysis and tumor growth. In conclusion, these findings suggest that circ235 may be a viable molecular marker and therapeutic target for Bca.
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