Skip to main content
. 2021 Jan 22;7:21. doi: 10.1038/s41420-020-00398-5

Fig. 5. ADO promotes glioma stemness via augmenting a NF-κB-CCL20 feedforward activation loop.

Fig. 5

a The concentrations of CCL20 generated from 6 groups were detected using Elisa: LN229 control group, cells treated with TNFα (2 μM), ADO-Cas9 cells, cells paired with NF-κB 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.