ArticleCancer research2017
SOX5/6/21 Prevent Oncogene-Driven Transformation of Brain Stem Cells.
Article in Cancer research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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
24 citing papers in PubMed, 46 citations in OpenAlex.
- Integrated Multiomic Profiling Identifies BRD8/EP400 as a Pivotal Chromatin Module Mediating Anti-HER2 Response in HR+/HER2+ Breast Cancer.Cancer research · 2026Article
- SOX21 suppresses glioblastoma growth by repressing AP-1 activity.Cell death & disease · 2026Article
- Sox5 controls cell cycle progression in intermediate progenitor cells during dentate gyrus development.Frontiers in cell and developmental biology · 2026Article
- DNMT1 blocks SOX21-repressed CKS2 transcription to promote gastric cancer progression.BMC cancer · 2025Article
- Role of the SOX family in cancer immune evasion: Emerging player and promising therapeutic opportunities.Medicine · 2025Review
- A cutting-edge investigation of the multifaceted role of SOX family genes in cancer pathogenesis through the modulation of various signaling pathways.Functional & integrative genomics · 2025Review
- Gene regulatory network topology governs resistance and treatment escape in glioma stem-like cells.Science advances · 2024Article
- Multifaceted roles and functions of SOX30 in human cancer.Cancer innovation · 2024Review
- A novel long non-coding RNA SLNCR1 promotes proliferation, migration, and invasion of melanoma via transcriptionally regulating SOX5.Cell death discovery · 2024Article
- SOX on tumors, a comfort or a constraint?Cell death discovery · 2024Review
- Article
- Effect of miR-499-5p/SOX6 axis on atrial fibrosis in rats with atrial fibrillation.Open medicine (Warsaw, Poland) · 2023Article
- NMilitary Medical Research · 2022Article
- Stanniocalcin-2 promotes cell EMT and glycolysis via activating ITGB2/FAK/SOX6 signaling pathway in nasopharyngeal carcinoma.Cell biology and toxicology · 2022Article
- SoxD genes are required for adult neural stem cell activation.Cell reports · 2022Article
- SOX transcription factors and glioma stem cells: Choosing between stemness and differentiation.World journal of stem cells · 2021Review
- SoxD transcription factor deficiency in Schwann cells delays myelination in the developing peripheral nervous system.Scientific reports · 2021Article
- Structural basis for nuclear import selectivity of pioneer transcription factor SOX2.Nature communications · 2021Article
- CYCLIN-B1/2 and -D1 act in opposition to coordinate cortical progenitor self-renewal and lineage commitment.Nature communications · 2020Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 1 institution in 1 country.
Funding
Abstract
Molecular mechanisms preventing self-renewing brain stem cells from oncogenic transformation are poorly defined. We show that the expression levels of SOX5, SOX6, and SOX21 (SOX5/6/21) transcription factors increase in stem cells of the subventricular zone (SVZ) upon oncogenic stress, whereas their expression in human glioma decreases during malignant progression. Elevated levels of SOX5/6/21 promoted SVZ cells to exit the cell cycle, whereas genetic ablation of SOX5/6/21 dramatically increased the capacity of these cells to form glioma-like tumors in an oncogene-driven mouse brain tumor model. Loss-of-function experiments revealed that SOX5/6/21 prevent detrimental hyperproliferation of oncogene expressing SVZ cells by facilitating an antiproliferative expression profile. Consistently, restoring high levels of SOX5/6/21 in human primary glioblastoma cells enabled expression of CDK inhibitors and decreased p53 protein turnover, which blocked their tumorigenic capacity through cellular senescence and apoptosis. Altogether, these results provide evidence that SOX5/6/21 play a central role in driving a tumor suppressor response in brain stem cells upon oncogenic insult.
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.