Siomycin A targets brain tumor stem cells partially through a MELK-mediated pathway

摘要: Glioblastoma multiforme (GBM) is a devastating disease, and the current therapies have only palliative effect. Evidence mounting to indicate that brain tumor stem cells (BTSCs) are minority of responsible for cancer initiation, propagation, maintenance. Therapies fail eradicate BTSCs may ultimately lead regrowth residual BTSCs. However, relatively resistant treatments. Development novel therapeutic strategies effectively BTSC are, therefore, essential. In previous study, we used patient-derived GBM sphere (stemlike cells) enrich identified maternal embryonic leucinezipper kinase (MELK) as key regulator survival stemlike in vitro. Here, demonstrate thiazole antibiotic, siomycin A, potently reduced MELK expression inhibited growth vivo. Treatment with A resulted arrested self-renewal, decreased invasion, induced apoptosis but had little effect on nonstem matched tumors or normal neural stem/progenitor cells. overexpression partially rescued phenotype A‐treated vivo, pretreatment abraded sizes cell‐derived immunodeficient mice. mice harboring intracranial significantly prolonged their period compared control Together, this study be first