ArticleOncotarget2016
Nuclear factor one B (NFIB) encodes a subtype-specific tumour suppressor in glioblastoma.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
26 citing papers in PubMed, 45 citations in OpenAlex.
- An ALKBH3 Inhibitor HUHS199 Suppresses Proliferation of Glioblastoma Cells by Targeting 1-Methyladenosine on GADD45A mRNA.Chemical biology & drug design · 2026Article
- Roles of the NFI/CTF gene family in transcription and development: update 2025.Academia biology · 2025Article
- Nuclear Factor I Family Members are Key Transcription Factors Regulating Gene Expression.Molecular & cellular proteomics : MCP · 2025Article
- PIN1 is a novel interaction partner and a negative upstream regulator of the transcription factor NFIB.FEBS letters · 2024Article
- A Patient Case of Malan Syndrome Involving 19p13.2 Deletion ofJournal of clinical medicine · 2024Article
- Integrated analysis of single-cell chromatin state and transcriptome identified common vulnerability despite glioblastoma heterogeneity.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Transcription Factor-Forced Astrocytic Differentiation Impairs Human Glioblastoma Growth In Vitro and In Vivo.Molecular cancer therapeutics · 2023Article
- Temporal and sequential transcriptional dynamics define lineage shifts in corticogenesis.The EMBO journal · 2022Article
- Transcriptional Regulation ofInternational journal of molecular sciences · 2022Article
- miR-18a promotes glioblastoma development by down-regulating ALOXE3-mediated ferroptotic and anti-migration activities.Oncogenesis · 2021Article
- Nuclear factor I/B mediates epithelial-mesenchymal transition in human melanoma cells through ZEB1.Oncology letters · 2021Article
- The Role of Neurodevelopmental Pathways in Brain Tumors.Frontiers in cell and developmental biology · 2021Review
- A circular RNA from NFIX facilitates oxidative stress-induced H9c2 cells apoptosis.In vitro cellular & developmental biology. Animal · 2020Article
- Voltage-gated ion channels mediate the electrotaxis of glioblastoma cells in a hybrid PMMA/PDMS microdevice.APL bioengineering · 2020Article
- Nuclear factor IX promotes glioblastoma development through transcriptional activation of Ezrin.Oncogenesis · 2020Article
- Transcription factors NFIA and NFIB induce cellular differentiation in high-grade astrocytoma.Journal of neuro-oncology · 2020Article
- Transcription levels and prognostic significance of the NFI family members in human cancers.PeerJ · 2020Article
- A positive feedback loop involving nuclear factor IB and calpain 1 suppresses glioblastoma cell migration.The Journal of biological chemistry · 2019Article
- A reference collection of patient-derived cell line and xenograft models of proneural, classical and mesenchymal glioblastoma.Scientific reports · 2019Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.