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Nonreceptor tyrosine kinase BMX maintains self-renewal and tumorigenic potential of glioblastoma stem cells by activating STAT3.
Glioblastomas display cellular hierarchies containing tumor-propagating glioblastoma stem cells (GSCs). STAT3 is a critical signaling node in GSC maintenance but molecular mechanisms underlying STAT3 activation in GSCs are poorly defined. Here we demonstrate that the bone marrow X-linked (BMX) nonreceptor tyrosine kinase activates STAT3 signaling to maintain self-renewal and tumorigenic potential of GSCs. BMX is differentially expressed in GSCs relative to nonstem cancer cells and neural progenitors. BMX knockdown potently inhibited STAT3 activation, expression of GSC transcription factors, and growth of GSC-derived intracranial tumors. Constitutively active STAT3 rescued the effects of BMX downregulation, supporting that BMX signals through STAT3 in GSCs. These data demonstrate that BMX represents a GSC therapeutic target and reinforces the importance of STAT3 signaling in stem-like cancer phenotypes.
Duke Scholars
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Related Subject Headings
- Vascular Endothelial Growth Factor A
- STAT3 Transcription Factor
- Receptors, Interleukin-6
- Protein-Tyrosine Kinases
- Oncology & Carcinogenesis
- Oligodendrocyte Transcription Factor 2
- Nerve Tissue Proteins
- Neoplastic Stem Cells
- Mice, Inbred C57BL
- Mice
Citation
![Journal cover image](https://secure.syndetics.com/index.aspx?isbn=/lc.gif&issn=1878-3686&client=dukeuniv)
Published In
DOI
EISSN
Publication Date
Volume
Issue
Start / End Page
Location
Related Subject Headings
- Vascular Endothelial Growth Factor A
- STAT3 Transcription Factor
- Receptors, Interleukin-6
- Protein-Tyrosine Kinases
- Oncology & Carcinogenesis
- Oligodendrocyte Transcription Factor 2
- Nerve Tissue Proteins
- Neoplastic Stem Cells
- Mice, Inbred C57BL
- Mice