Fig 1: ADO promotes glioma stemness via augmenting a NF-?B-CCL20 feedforward activation loop.a The concentrations of CCL20 generated from 6 groups were detected using Elisa: LN229 control group, cells treated with TNFa (2 µM), ADO-Cas9 cells, cells paired with NF-?B inhibitor BAY11-7082 (2 µM), ADO-Cas9 cells companied by hypotaurine (2 mM), BAY11-7082 companied by hypotaurine (2 mM). b Serial sections from patients were used to study ADO, CCL20, and CCR6 expression by immunohistochemistry. Scale bars = 50 µm. Representative staining patterns are shown. c Western blot analysis of ADO expression in 10 glioma patients. Cerebrospinal fluid was collected from these 10 glioma patients with varying ADO levels to test for intracranial CCL20, CXCL1, CXCL2, CXCL5, and CXCL16 levels using Luminex assays (R&D Systems). d The concentrations of CCL20 were compared between in glioma patients and nontumor patients, and also in patients with high and low levels of ADO. Data represent three independent experiments with similar results. Student’s t-test, *p < 0.05, **p < 0.01.
Fig 2: Inhibiting ADO attenuates glioblastoma growth in vivo.a LN229 ADO-Cas9 and control cells were injected into an orthotopical mouse xenograft model to analyze for in vivo tumor growth. Scale bars = 100 µm and 500 µm. b CCL20 and CCR6 expression were evaluated by immunohistochemistry in the xenograft tumors. Scale bars = 50 µm and 200 µm. Data represent three independent experiments with similar results.
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