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Inositol treatment inhibits medulloblastoma through suppression of epigenetic-driven metabolic adaptation
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Inositol treatment inhibits medulloblastoma through suppression of epigenetic-driven metabolic adaptation
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Journal Article
Inositol treatment inhibits medulloblastoma through suppression of epigenetic-driven metabolic adaptation
2021
Overview
Deregulation of chromatin modifiers plays an essential role in the pathogenesis of medulloblastoma, the most common paediatric malignant brain tumour. Here, we identify a BMI1-dependent sensitivity to deregulation of inositol metabolism in a proportion of medulloblastoma. We demonstrate mTOR pathway activation and metabolic adaptation specifically in medulloblastoma of the molecular subgroup G4 characterised by a BMI1
High
;CHD7
Low
signature and show this can be counteracted by IP6 treatment. Finally, we demonstrate that IP6 synergises with cisplatin to enhance its cytotoxicity in vitro and extends survival in a pre-clinical BMI1
High
;CHD7
Low
xenograft model.
BMI1 and CHD7 are chromatin remodelling genes with a role in medulloblastoma pathogenesis. Here, the authors demonstrate that the BMI1
High
/CHD7
Low
signature mediates metabolic adaptation in G4 MB and predicts response to inositol treatment either alone or in combination with chemotherapy.
Publisher
Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio
Subject
/ 13/100
/ 14/63
/ 38
/ 45
/ 45/91
/ 64/60
/ 82/80
/ 96/106
/ 96/95
/ Adaptation, Physiological - drug effects
/ Animals
/ Cell Proliferation - drug effects
/ Cell Survival - drug effects
/ Cerebellar Neoplasms - genetics
/ DNA-Binding Proteins - metabolism
/ Epigenesis, Genetic - drug effects
/ Humanities and Social Sciences
/ Humans
/ Inositol
/ Mice
/ Neural Stem Cells - metabolism
/ Oxygen Consumption - drug effects
/ Phosphatidylinositols - metabolism
/ Polycomb Repressive Complex 1 - metabolism
/ Promoter Regions, Genetic - genetics
/ Proto-Oncogene Proteins - metabolism
/ Science
/ TOR Serine-Threonine Kinases - metabolism
/ Toxicity
