Nuclear factor one B (<i>NFIB</i>) encodes a subtype-specific tumour suppressor in glioblastoma

Stringer, Brett W.; Bunt, Jens; Day, Bryan W.; Barry, Guy; Jamieson, Paul; Ensbey, Kathleen S.; Bruce, Zara C.; Goasdoué, Kate; Vidal, Hélène; Charmsaz, Sara; Smith, Fiona; Cooper, Leanne; Piper, Michael; Boyd, Andrew W.; Richards, Linda J.

doi:10.18632/oncotarget.8720

Cited by 36 publications

(46 citation statements)

References 77 publications

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“…For example, it has been suggested that NFIA is involved in the neuroprotection of neurons following administration of sub‐lethal doses of N‐methyl‐D‐aspartate (Zheng et al, ) and inhibition of remyelination in human myelin disorders via regulation of oligodendrocyte progenitor differentiation (Fancy et al, ). NFI proteins have also been implicated in mental disorders, such as autism (Chuang et al, ; Tsang et al, ) and bipolar disorder (Le‐Niculescu et al, ), as well as multiple sclerosis (Fancy et al, ), Parkinson's disease (Suwarnalata et al, ), and brain tumours (Genovesi et al, ; Glasgow et al, ; Ho et al, ; Idbaih et al, ; Lacroix et al, ; Lastowska et al, ; Lee et al, ; Song et al, ; Stringer et al, ; Vyazunova et al, ). The NFI expression pattern in the adult cortex provides a basis for investigating their function in these diseases, and identifying the cell types involved.…”

Section: Discussionmentioning

confidence: 99%

“…The NFI expression pattern in the adult cortex provides a basis for investigating their function in these diseases, and identifying the cell types involved. For instance, NFIA (Glasgow et al, ; Lee et al, ; Song et al, ; Vyazunova et al, ) and NFIB (Idbaih et al, ; Stringer et al, ) are both associated with the progression of glioma, a brain cancer of astrocytic origin. Future studies using cell type‐specific and/or inducible deletion of NFI proteins will be required to delineate their precise role in these cell types in order to understand the full extent of their post‐developmental role.…”

Section: Discussionmentioning

confidence: 99%

“…Considering that NFI proteins have recently been implicated in diseases such as autism and cancer (Chuang, Huang, & Hsueh, ; Fancy, Glasgow, Finley, Rowitch, & Deneen, ; Genovesi et al, ; Glasgow et al, ; Ho et al, ; Idbaih et al, ; Lacroix et al, ; Lastowska et al, ; Le‐Niculescu et al, ; Lee et al, ; Song et al, ; Stringer et al, ; Suwarnalata et al, ; Tsang et al, ; Vyazunova et al, ), a thorough analysis of their expression in the adult brain is required. Here, we examined both region and cell‐type‐specific expression in the adult mouse cerebral cortex using antibodies specific for NFIA, NFIB, and NFIX.…”

Section: Introductionmentioning

confidence: 99%

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Differential neuronal and glial expression of nuclear factor I proteins in the cerebral cortex of adult mice

Chen

Harris

Lim

et al. 2017

J of Comparative Neurology

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The nuclear factor I (NFI) family of transcription factors plays an important role in the development of the cerebral cortex in humans and mice. Disruption of nuclear factor IA (NFIA), nuclear factor IB (NFIB), or nuclear factor IX (NFIX) results in abnormal development of the corpus callosum, lateral ventricles, and hippocampus. However, the expression or function of these genes has not been examined in detail in the adult brain, and the cell type-specific expression of NFIA, NFIB, and NFIX is currently unknown. Here, we demonstrate that the expression of each NFI protein shows a distinct laminar pattern in the adult mouse neocortex and that their cell type-specific expression differs depending on the family member. NFIA expression was more frequently observed in astrocytes and oligodendroglia, whereas NFIB expression was predominantly localized to astrocytes and neurons. NFIX expression was most commonly observed in neurons. The NFI proteins were equally distributed within microglia, and the ependymal cells lining the ventricles of the brain expressed all three proteins. In the hippocampus, the NFI proteins were expressed during all stages of neural stem cell differentiation in the dentate gyrus, with higher expression intensity in neuroblast cells as compared to quiescent stem cells and mature granule neurons. These findings suggest that the NFI proteins may play distinct roles in cell lineage specification or maintenance, and establish the basis for further investigation of their function in the adult brain and their emerging role in disease.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Differential neuronal and glial expression of nuclear factor I proteins in the cerebral cortex of adult mice

Chen

Harris

Lim

et al. 2017

J of Comparative Neurology

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“…Glioblastoma can be molecularly classified into proneural, neural, classical, and mesenchymal types according to The Cancer Genome Atlas (TCGA) 36 . We use two glioblastoma cell models, T98G and U-251MG, which are both of caucasian male origin and classified as mesenchymal type with p53 mutant genotype 37,38 . The adhesion and electrotaxis of T98G and U-251MG glioblastoma cell lines on various ECMs are tested in a double-layer hybrid multiple electric field chip (HMEFC) based on the hybrid PMMA/PDMS design approach 17 (Supplementary TABLE. S.1).…”

Section: B Glioblastoma Electrotaxis Requires Optimal Laminin-contaimentioning

confidence: 99%

“…Both T98G cells and U-251MG cells are categorized as mesenchymal type glioblastoma 37,38 , however, their electrotactic responses are completely different. Similar results are reported in the electrotaxis of glioblastoma cells and spheroids 15,16,19,39 and lung adenocarcinoma 51 , showing that although molecular and surface marker makeups of the cell lines are similar, their electrotaxis responses can be completely different.…”

Section: Electrotaxis Behavior May Reflect the Heterogeneity Of Glmentioning

confidence: 99%

Voltage-gated ion channels mediate the electrotaxis of glioblastoma cells in a hybrid PMMA/PDMS microdevice

Tsai

IJspeert

Shen

2020

Preprint

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Transformed astrocytes in the most aggressive form cause glioblastoma, the most common cancer in central nervous system with high mortality. The physiological electric field by neuronal local field potentials and tissue polarity may guide the infiltration of glioblastoma cells through the electrotaxis process. However, microenvironments with multiplex gradients are difficult to create. In this work, we have developed a hybrid microfluidic platform to study glioblastoma electrotaxis in controlled microenvironments with high throughput quantitative analysis by a machine learning-powered single cell tracking software. By equalizing the hydrostatic pressure difference between inlets and outlets of the microchannel, uniform single cells can be seeded reliably inside the microdevice. The electrotaxis of two glioblastoma models, T98G and U-251MG, require optimal laminin-containing extracellular matrix and exhibits opposite directional and electro-alignment tendencies. Calcium signaling is a key contributor in glioblastoma pathophysiology but its role in glioblastoma electrotaxis is still an open question. Anodal T98G electrotaxis and cathodal U-251MG electrotaxis require the presence of extracellular calcium cations. U-251MG electrotaxis is dependent on the P/Q-type voltage-gated calcium channel (VGCC) and T98G is dependent on the R-type VGCC. U-251MG and T98G electrotaxis are also mediated by A-type (rapidly inactivating) voltage-gated potassium channels and acidsensing sodium channels. The involvement of multiple ion channels suggests that the glioblastoma electrotaxis is complex and patient-specific ion channel expression can be critical to develop personalized therapeutics to fight against cancer metastasis. The hybrid microfluidic design and machine learning-powered single cell analysis provide a simple and flexible platform for quantitative investigation of complicated biological systems.

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Nuclear factor one transcription factors as epigenetic regulators in cancer

Fane

Harris

Smith

et al. 2017

Intl Journal of Cancer

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Tumour heterogeneity poses a distinct obstacle to therapeutic intervention. While the initiation of tumours across various physiological systems is frequently associated with signature mutations in genes that drive proliferation and bypass senescence, increasing evidence suggests that tumour progression and clonal diversity is driven at an epigenetic level. The tumour microenvironment plays a key role in driving diversity as cells adapt to demands imposed during tumour growth, and is thought to drive certain subpopulations back to a stem cell-like state. This stem cell-like phenotype primes tumour cells to react to external cues via the use of developmental pathways that facilitate changes in proliferation, migration and invasion. Because the dynamism of this stem cell-like state requires constant chromatin remodelling and rapid alterations at regulatory elements, it is of great therapeutic interest to identify the cell-intrinsic factors that confer these epigenetic changes that drive tumour progression. The nuclear factor one (NFI) family are transcription factors that play an important role in the development of many mammalian organ systems. While all four family members have been shown to act as either oncogenes or tumour suppressors across various cancer models, evidence has emerged implicating them as key epigenetic regulators during development and within tumours. Notably, NFIs have also been shown to regulate chromatin accessibility at distal regulatory elements that drive tumour cell dissemination and metastasis. Here we summarize the role of the NFIs in cancer, focusing largely on the potential mechanisms associated with chromatin remodelling and epigenetic modulation of gene expression.

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Nuclear factor one B (NFIB) encodes a subtype-specific tumour suppressor in glioblastoma

Cited by 36 publications

References 77 publications

Differential neuronal and glial expression of nuclear factor I proteins in the cerebral cortex of adult mice

Differential neuronal and glial expression of nuclear factor I proteins in the cerebral cortex of adult mice

Voltage-gated ion channels mediate the electrotaxis of glioblastoma cells in a hybrid PMMA/PDMS microdevice

Nuclear factor one transcription factors as epigenetic regulators in cancer

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