Journal
ONCOGENE
Volume 37, Issue 31, Pages 4313-4333Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/s41388-018-0277-1
Keywords
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Funding
- Brain Tumour Charity UK (BTC) [8/128]
- Centre grant from BTC [8/197]
- Brain Tumour Research UK
- Department of Health's NIHR Biomedical Research Centre's funding scheme
- CRUK Accelerator Ed-UCL Grant [C416/A23615]
- University College London (Overseas research scholarship, UCL ORS)
- UCLH Charity
- Cancer Research UK [C1 15121 A 20256]
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To identify biomarkers for glioma growth, invasion and progression, we used a candidate gene approach in mouse models with two complementary brain tumour phenotypes, developing either slow-growing, diffusely infiltrating gliomas or highly proliferative, non-invasive primitive neural tumours. In a microRNA screen we first identified microRNA-449a as most significantly differentially expressed between these two tumour types. miR-449a has a target dependent effect, inhibiting cell growth and migration by downregulation of CCND1 and suppressing neural phenotypes by inhibition of G protein coupled-receptor (GPR) 158. GPR158 promotes glioma stem cell differentiation and induces apoptosis and is highest expressed in the cerebral cortex and in oligodendrogliomas, lower in IDH mutant astrocytomas and lowest in the most malignant form of glioma, IDH wild-type glioblastoma. The correlation of GPR158 expression with molecular subtypes, patient survival and therapy response suggests a possible role of GPR158 as prognostic biomarker in human gliomas.
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