Human VCAN(Versican core protein) ELISA Kit

The oncogenesis and progression of gastric cancer are closely correlated with the complex regulatory relationships among messenger RNA (mRNA), long noncoding RNA (lncRNA), and microRNA (miRNA). After constructing the gastric cancer lncRNA-miRNA-mRNA regulatory network, we analyzed the network topology properties and found that lncRNA ADAMTS9-AS2 and C20orf166-AS1 and miRNA hsa-mir-204 are key nodes. Further functional enrichment analysis and survival analysis were performed on these key nodes and the RNAs interacting with them. We found that CHRM2, ANGPT2, and COL1A1 interacting with ADAMTS9-AS2 are enriched in the PI3K-Akt signaling pathway, and low expression of the ADAMTS9-AS2 is closely related to the prognosis of patients. Abnormal expression of CACNA1H, FLNA, and FLNC interacting with lncRNA C20orf166-AS1 is associated with MAPK signaling pathway in gastric cancer. In addition, the downregulated miRNA hsa-mir-204 promotes invasion and proliferation of gastric cancer cells by regulating the abnormal expression of mRNAs (CHRDL1 and NPTX1) and lncRNAs (ADAMTS9-AS2, NKX2-1-AS1, TLR8-AS1, and VCAN-AS1). This study systematically analyzed the lncRNA-miRNA-mRNA regulatory network of gastric cancer, which not only has a new understanding of the pathogenesis of gastric cancer, but also provides new insights for the early diagnosis and treatment of gastric cancer.

Growing evidence suggests that versican is important in the innate immune response to lung infection. Our goal was to understand the regulation of macrophage-derived versican and the role it plays in innate immunity. We first defined the signaling events that regulate versican expression, using bone marrow-derived macrophages (BMDMs) from mice lacking specific Tolllike receptors (TLRs), TLR adaptor molecules, or the type I interferon receptor (IFNAR1). We show that LPS and polyinosinic-polycytidylic acid [poly(I: C)] trigger a signaling cascade involving TLR3 or TLR4, the Trif adaptor, type I interferons, and IFNAR1, leading to increased expression of versican by macrophages and implicating versican as an interferon-stimulated gene. The signaling events regulating versican are distinct from those for hyaluronan synthase 1 (HAS1) and syndecan-4 in macrophages. HAS1 expression requires TLR2 and MyD88. Syndecan-4 requires TLR2, TLR3, or TLR4 and both MyD88 and Trif. Neither HAS1 nor syndecan-4 is dependent on type I interferons. The importance of macrophage-derived versican in lungs was determined with LysM/Vcan(-/-) mice. These studies show increased recovery of inflammatory cells in the bronchoalveolar lavage fluid of poly(I: C)-treated LysM/Vcan(-/-) mice compared with control mice. IFN-beta and IL-10, two important anti-inflammatory molecules, are significantly decreased in both poly(I: C)-treated BMDMs from LysM/Vcan(-/-) mice and bronchoalveolar lavage fluid from poly(I: C)treated LysM/Vcan(-/-) mice compared with control mice. In short, type I interferon signaling regulates versican expression, and versican is necessary for type I interferon production. These findings suggest that macrophage-derived versican is an immunomodulatory molecule with anti-inflammatory properties in acute pulmonary inflammation.