The present study investigated the underlying molecular mechanism by which Buthus martensii Karsch chlorotoxin (BmK CT) inhibits the invasion and metastasis of glioma cells and the possibility of 131I-labeled BmK… Click to show full abstract
The present study investigated the underlying molecular mechanism by which Buthus martensii Karsch chlorotoxin (BmK CT) inhibits the invasion and metastasis of glioma cells and the possibility of 131I-labeled BmK CT (131I-BmK CT) as a novel targeted agent for the treatment of glioma. The impact of BmK CT with and without 131I radiolabeling on the invasion and metastasis of glioma cells in vitro was studied. Cell viability was assessed using Cell Counting Kit-8 and plate colony formation assays in order to confirm the cytotoxicity of BmK CT and 131I-BmK CT at different concentrations. Transwell invasion and wound-healing assays were conducted in order to investigate the inhibitory effects BmK CT and 131I-BmK CT on cell migration and invasion. Furthermore, western blotting, ELISA immunofluorescence and a gelatin zymography assay were performed to evaluate changes in the protein expression levels of glioma cells following treatment with BmK CT or 131I-BmK CT. The results indicated that BmK CT inhibits the invasion and metastasis of glioma cells via regulation of tissue inhibitor of metalloproteinase-2 expression and that 131I-BmK CT has the potential to be a novel targeted therapeutic drug for glioma.
               
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