| Objective: CXCL1 is a member of the CXC chemokine family,which not only participates in the activation of immune cells,but also in many cellular reactions.Recent studies have shown that the expression of CXCL1 is up-regulated in many human tumors and is involved in the proliferation,metastasis of tumor cells and angiogenesis of tumor.The aim of this study is to investigate the expression of CXCL1 in human brain glioma,and the effect and mechanism of recombinant exogenous CXCL1 on the proliferation and migration of rat C6 brain glioma cells.The current may provide a potential marker or molecular target for the diagnosis and treatment of the disease.Methods: The Cancer Genome Atlas(TCGA)database was used to compare the m RNA levels of CXCL1 gene between human normal brain and brain glioma tissues.The relationship between the expression of CXCL1 gene and the survival prognosis of patients with brain glioma was analyzed by Kaplan-Meier survival method;Gene set enrichment analysis(GSEA)was used to investigate the possible signal pathways involved in CXCL1 in brain gliomas.The effects of different concentrations of CXCL1 on the proliferation of rat C6 brain glioma cells were studied by using CCK-8 Cell proliferation sssay.Transwell cell migration assay was used to study the effects of different concentration of recombinant CXCL1 on the migration activity of rat C6 brain glioma cells.Western blot was used to study the effects of different concentrations of CXCL1 on the expression of BAX and ERK in rat C6 brain glioma cells.Results: The CGGA analysis showed that CXCL1 m RNA levels in human brain glioma tissues were significantly higher than those in normal control tissues.Kaplan-Meier survival analysis showed that the survival time of brain glioma patients with high expression of CXCL1 was significantly shorter than those with low expression of CXCL1.The Kyoto Encyclopedia of Genes and Genomes(KEGG)signal pathway enrichment analysis showed that CXCL1 is highly enriched in the cytokine-cytokine receptor interaction pathway,cell adhesion molecules pathway,apoptosis pathway,natural killer cell-mediated cytotoxicity pathway,Nod-like receptor signaling pathway and chemokine signaling pathway.At 72 h after incubation of C6 cells with different concentrations of CXCL1,the results from CCK-8 cell proliferation assay demonstrated that the proliferation activity of C6 cells treated with 5 ng/ml,10 ng/ml,20 ng/ml,30 ng/ml or 50 ng/ml CXCL1 was obviously enhanced as compared with C6 cells treated with 5ng/ml CXCL1.After 24 h incubation of C6 cells with different concentrations of CXCL1,the data from transwell cell migration assay showed that treatment with 10 ng/ml,20 ng/ml,30ng/ml or 50 ng/ml CXCL1 predominantly promoted C6 cells migration ability relative to C6 cells treated with 0 ng/ml CXCL1.Western blot analysis showed that the expression levels of BAX in C6 cells treated with 50 ng/ml recombinant CXCL1 were remarkably down-regulated,whereas ERK protein in C6 cells treated with 20 ng/ml and 50 ng/ml recombinant CXCL1 was significantly up-regulated,as compared with those treated with 0 ng/ml CXCL1.Conclusion: The expression of CXCL1 was up-regulated in human brain gliomas,and the high expression of CXCL1 was related to the short-term survival of patients with brain gliomas.Exogenous recombinant CXCL1 may participate in the malignant transformation of rat C6 brain glioma cells through MAPK / ERK/BAX signal transduction pathway. |
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