ArticleNeuro-oncology2011
Siomycin A targets brain tumor stem cells partially through a MELK-mediated pathway.
Article in Neuro-oncology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 59 citations in OpenAlex.
- The role of MELK in cancer: mechanisms and therapeutic options.Frontiers in oncology · 2026Review
- Targeting PGM3 abolishes SREBP-1 activation-hexosamine synthesis feedback regulation to effectively suppress brain tumor growth.Science advances · 2025Article
- Targeting MELK in tumor cells and tumor microenvironment: from function and mechanism to therapeutic application.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025Review
- CPI203, a BET inhibitor, down-regulates a consistent set of DNA synthesis genes across a wide array of glioblastoma lines.PloS one · 2025Article
- Melk facilitates pulmonary artery smooth muscle cell proliferation and migration in pulmonary hypertension via modulation of YAP/TAZ signaling.Frontiers in cell and developmental biology · 2025Article
- P4HA2 promotes cell proliferation and migration in glioblastoma.Oncology letters · 2021Article
- Siomycin A induces reactive oxygen species-mediated cytotoxicity in ovarian cancer cells.Oncology letters · 2021Article
- Identification of ALDH1A3 as a Viable Therapeutic Target in Breast Cancer Metastasis-Initiating Cells.Molecular cancer therapeutics · 2020Article
- MEK/MELK inhibition and blood-brain barrier deficiencies in atypical teratoid/rhabdoid tumors.Neuro-oncology · 2020Article
- Effects and mechanism of siomycin A on the growth and apoptosis of MiaPaCa-2 cancer cells.Oncology letters · 2019Article
- EZH2 Phosphorylation Promotes Self-Renewal of Glioma Stem-Like Cells Through NF-κB Methylation.Frontiers in oncology · 2019Article
- Maternal embryonic leucine zipper kinase is a novel target for proliferation-associated high-risk myeloma.Haematologica · 2018Article
- Phosphorylation of the HIV-1 capsid by MELK triggers uncoating to promote viral cDNA synthesis.PLoS pathogens · 2017Article
- FOXD1-ALDH1A3 Signaling Is a Determinant for the Self-Renewal and Tumorigenicity of Mesenchymal Glioma Stem Cells.Cancer research · 2016Article
- Article
- Senescence from glioma stem cell differentiation promotes tumor growth.Biochemical and biophysical research communications · 2016Article
- Gene expression profiling distinguishes proneural glioma stem cells from mesenchymal glioma stem cells.Genomics data · 2015Article
- Kinome-wide shRNA screen identifies the receptor tyrosine kinase AXL as a key regulator for mesenchymal glioblastoma stem-like cells.Stem cell reports · 2015Article
- EZH2 protects glioma stem cells from radiation-induced cell death in a MELK/FOXM1-dependent manner.Stem cell reports · 2015Article
- Crosstalk between glioma-initiating cells and endothelial cells drives tumor progression.Cancer research · 2014Article
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
Abstract
Glioblastoma multiforme (GBM) is a devastating disease, and the current therapies have only palliative effect. Evidence is mounting to indicate that brain tumor stem cells (BTSCs) are a minority of tumor cells that are responsible for cancer initiation, propagation, and maintenance. Therapies that fail to eradicate BTSCs may ultimately lead to regrowth of residual BTSCs. However, BTSCs are relatively resistant to the current treatments. Development of novel therapeutic strategies that effectively eradicate BTSC are, therefore, essential. In a previous study, we used patient-derived GBM sphere cells (stemlike GBM cells) to enrich for BTSC and identified maternal embryonic leucine-zipper kinase (MELK) as a key regulator of survival of stemlike GBM cells in vitro. Here, we demonstrate that a thiazole antibiotic, siomycin A, potently reduced MELK expression and inhibited tumor growth in vivo. Treatment of stemlike GBM cells with siomycin A resulted in arrested self-renewal, decreased invasion, and induced apoptosis but had little effect on growth of the nonstem cells of matched tumors or normal neural stem/progenitor cells. MELK overexpression partially rescued the phenotype of siomycin A-treated stemlike GBM cells. In vivo, siomycin A pretreatment abraded the sizes of stemlike GBM cell-derived tumors in immunodeficient mice. Treatment with siomycin A of mice harboring intracranial tumors significantly prolonged their survival period compared with the control mice. Together, this study may be the first model to partially target stemlike GBM cells through a MELK-mediated pathway with siomycin A to pave the way for effective treatment of GBM.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.