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Abstract
Glioblastoma (GBM) is an essentially incurable and rapidly fatal cancer, with few markers predicting a favourable prognosis. Here we report that the transcription factor NFIB is associated with significantly improved survival in GBM. NFIB expression correlates inversely with astrocytoma grade and is lowest in mesenchymal GBM. Ectopic expression of NFIB in low-passage, patient-derived classical and mesenchymal subtype GBM cells inhibits tumourigenesis. Ectopic NFIB expression activated phospho-STAT3 signalling only in classical and mesenchymal GBM cells, suggesting a mechanism through which NFIB may exert its context-dependent tumour suppressor activity. Finally, NFIB expression can be induced in GBM cells by drug treatment with beneficial effects.
Highlights
Glioblastoma (GBM; WHO grade IV astrocytoma) is the most common, and most lethal, primary malignant cancer of the central nervous system [1]
We analysed whether NFIB expression correlated with these subtypes using data from The Cancer Genome Atlas (TCGA) dataset of patient tumour tissue, classified as either proneural, neural, classical or mesenchymal GBM [25,26,27]
We found NFIB expression was lowest in mesenchymal GBM and highest in proneural GBM (Figure 1E)
Summary
Glioblastoma (GBM; WHO grade IV astrocytoma) is the most common, and most lethal, primary malignant cancer of the central nervous system [1]. Many genetic alterations and gene expression changes have been reported for GBM, yet those that contribute significantly to cellular transformation in this disease remain to be defined, as are informative molecular biomarkers that predict patient prognosis. Ectopic overexpression of NFIB in the spinal cord induces precocious astrogliogenesis [12] These studies suggest that NFI genes play a key role in the transition of proliferating progenitor cells to differentiated astrocytes. Nfib was identified in insertional mutagenesis mouse screens designed to identify genes that, when mutated, increase the likelihood of developing GBM or other brain tumours [17,18,19,20] Taken together, these observations underscore the possibility that as an inducer of astrocyte differentiation, NFIB could function as a tumour suppressor in astrocytic tumours. We investigated the function of NFIB in human GBM and the potential clinical relevance of NFIB as a tumour suppressor in GBM biology
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