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https://www.selleckchem.com/products/namodenoson-cf-102.html Sphingosine kinase 1 (SphK1) is a potential therapeutic target for human osteosarcoma (OS). SphK1-targeting microRNAs (miRNAs) could have important therapeutic value for OS. We discovered that micorRNA-3677 (miR-3677) is a SphK1-targeting miRNA, inhibiting OS cell progression. The results of RNA-Pull down assay confirmed direct binding between biotinylated-miR-3677 and SphK1 mRNA in primary human OS cells. In established and primary human OS cells forced overexpression of miR-3677, by a lentiviral construct, decreased SphK1 3'-UTR (untranslated region) activity and downregulated SphK1 expression. Both were however enhanced with miR-3677 inhibition in OS cells. Function studies demonstrated that OS cell growth, proliferation and migration were inhibited with miR-3677 overexpression, but augmented with miR-3677 inhibition. MiR-3677 overexpression-induced anti-OS cell activity was reversed with re-expression of the 3'-UTR-depleted SphK1. Additionally, in SphK1 knockout OS cells (by CRISPR/Cas9 strategy), altering miR-3677 expression failed to further alter cell functions. Finally, we show that miR-3677 expression was significantly downregulated in primary human OS tissues, correlating with SphK1 mRNA upregulation. We conclude that targeting SphK1 by miR-3677 inhibits human OS cell progression.Macrophages control the initiation and resolution of cardiac fibrosis in post-infarction cardiac remodeling. The aim of the present study was to investigate whether N-propargyl caffeate amide (PACA) could suppress myocardial fibrosis via regulating macrophage polarization. By using rat model of isoproterenol-induced myocardial fibrosis, we discovered that PACA could reduce cardiac fibrosis in a dose-dependent manner. To elucidate the anti-fibrotic mechanisms, we examined whether PACA affected pro-inflammatory M1 and pro-resolving macrophage biomarkers in macrophage polarization. As result, PACA reduced the expression of
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