ArticleBMC neurology2014
SOX4 inhibits GBM cell growth and induces G0/G1 cell cycle arrest through Akt-p53 axis.
Article in BMC neurology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
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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.
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Who cites it
28 citing papers in PubMed, 41 citations in OpenAlex.
- Unrevealing the dual role of paired box and sex determining region Y related high mobility group box in glioblastoma.Discover oncology · 2026Review
- Targeting ESM1 via SOX4 promotes the progression of infantile hemangioma through the PI3K/AKT signaling pathway.Precision clinical medicine · 2024Article
- Single-cell multi-omics identify novel regulators required for osteoclastogenesis during aging.iScience · 2024Article
- Gene regulatory network topology governs resistance and treatment escape in glioma stem-like cells.Science advances · 2024Article
- Network Pharmacology and Bioinformatics Analysis to Identify the Molecular Targets and its Biological Mechanisms of Sciadopitysin against Glioblastoma.Journal of Cancer · 2024Article
- Transfer RNAs as dynamic and critical regulators of cancer progression.Nature reviews. Cancer · 2023Review
- Crosstalk betweenInternational journal of molecular sciences · 2023Review
- UBE2T promotes glioblastoma malignancy through ubiquitination-mediated degradation of RPL6.Cancer science · 2023Article
- WDR5 represents a therapeutically exploitable target for cancer stem cells in glioblastoma.Genes & development · 2023Article
- Interplay of SOX transcription factors and microRNAs in the brain under physiological and pathological conditions.Neural regeneration research · 2022Review
- tRNA Function and Dysregulation in Cancer.Frontiers in cell and developmental biology · 2022Review
- The Role of Micro RNAs in Regulating PI3K/AKT Signaling Pathways in Glioblastoma.Iranian journal of pathology · 2022Review
- The Roles of FHL3 in Cancer.Frontiers in oncology · 2022Review
- SOX transcription factors and glioma stem cells: Choosing between stemness and differentiation.World journal of stem cells · 2021Review
- Interplay of mClinical and translational medicine · 2021Article
- Alternate Roles of Sox Transcription Factors beyond Transcription Initiation.International journal of molecular sciences · 2021Review
- The Role of Neurodevelopmental Pathways in Brain Tumors.Frontiers in cell and developmental biology · 2021Review
- SOX4-mediated repression of specific tRNAs inhibits proliferation of human glioblastoma cells.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- SOX2 protein biochemistry in stemness, reprogramming, and cancer: the PI3K/AKT/SOX2 axis and beyond.Oncogene · 2020Review
- MicroRNA-130a modulates a radiosensitivity of rectal cancer by targeting SOX4.Neoplasia (New York, N.Y.) · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSOX4 is a transcription factor required for tissue development and differentiation in vertebrates. Overexpression of SOX4 has been reported in many cancers including glioblastoma multiforme (GBM), however, the underlying mechanism of actions has not been studied. In this study, we investigated the role of SOX4 in GBM.
methodsKaplan-Meier analysis was performed to assess the association between SOX4 expression levels and survival times in primary GBM samples. Cre/lox P system was used to generate gain or loss of SOX4 in GBM cells, and microarray analysis uncovered the regulation network of SOX4 in GBM cells.
resultsHigh SOX4 expression was significantly associated with good prognosis of primary GBMs. SOX4 inhibited the growth of GBM cell line LN229, A172G and U87MG, partly via the activation of p53-p21 signaling and down-regulation of phosphorylated AKT1. Gene expression profiling and subsequent gene ontology analysis showed that SOX4 influenced several key pathways including the Wnt/ beta-catenin and TGF-beta signaling pathways.
conclusionsOur study found that SOX4 acts as a tumor suppressor in GBM cells by induce cell cycle arrest and inhibiting cell growth.
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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.