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Anti-metastatic effect of (131)I-labeled Buthus martensii Karsch chlorotoxin in gliomas

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 (131)I-labeled BmK CT ((131)I-BmK CT) as a novel targeted agent for the treatment of glioma. The impact...

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Detalles Bibliográficos
Autores principales: Wu, Shan, Ma, Ke, Qiao, Wen-Li, Zhao, Ling-Zhou, Liu, Chang-Cun, Guo, Li-Lei, Xing, Yan, Zhu, Mei-Lin, Zhao, Jin-Hua
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6202110/
https://www.ncbi.nlm.nih.gov/pubmed/30272348
http://dx.doi.org/10.3892/ijmm.2018.3905
Descripción
Sumario: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 (131)I-labeled BmK CT ((131)I-BmK CT) as a novel targeted agent for the treatment of glioma. The impact of BmK CT with and without (131)I 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 (131)I-BmK CT at different concentrations. Transwell invasion and wound-healing assays were conducted in order to investigate the inhibitory effects BmK CT and (131)I-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 (131)I-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 (131)I-BmK CT has the potential to be a novel targeted therapeutic drug for glioma.