ArticleOncotarget2016
HMGA2 sustains self-renewal and invasiveness of glioma-initiating cells.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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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
19 citing papers in PubMed.
- HMGA proteins in the nervous system: role in brain tumorigenesis and neurodegeneration.Cell death discovery · 2026Review
- Phenotypic variations in glioma stem cells: regulatory mechanisms and implications for therapeutic strategies.Journal of translational medicine · 2025Review
- An engineered tumor organoid model reveals cellular identity and signaling trajectories underlying SFPQ-TFE3 driven translocation RCC.iScience · 2025Article
- Targeting stromal cells in tumor microenvironment as a novel treatment strategy for glioma.Cancer cell international · 2025Review
- Forkhead box transcription factors (FOXOs and FOXM1) in glioma: from molecular mechanisms to therapeutics.Cancer cell international · 2023Review
- LIN28B and Let-7 in Diffuse Midline Glioma: A Review.Cancers · 2023Review
- Resolving the lineage relationship between malignant cells and vascular cells in glioblastomas.Protein & cell · 2023Article
- Review
- SATB2 drives glioblastoma growth by recruiting CBP to promote FOXM1 expression in glioma stem cells.EMBO molecular medicine · 2020Article
- HMGA2-mediated tumorigenesis through angiogenesis in leiomyoma.Fertility and sterility · 2020Article
- HMGA Genes and Proteins in Development and Evolution.International journal of molecular sciences · 2020Review
- HIT000218960 promotes gastric cancer cell proliferation and migration through upregulation of HMGA2 expression.Oncology letters · 2019Article
- Molecular Determinants of Malignant Brain Cancers: From Intracellular Alterations to Invasion Mediated by Extracellular Vesicles.International journal of molecular sciences · 2017Review
- Clinicopathological and prognostic significance of SDC1 overexpression in breast cancer.Oncotarget · 2017Article
- CECR1-mediated cross talk between macrophages and vascular mural cells promotes neovascularization in malignant glioma.Oncogene · 2017Article
- Dovitinib enhances temozolomide efficacy in glioblastoma cells.Molecular oncology · 2017Article
- Article
- Cell-based high-throughput compound screening reveals functional interaction between oncofetal HMGA2 and topoisomerase I.Nucleic acids research · 2016Article
- Glioblastoma Stem-Like Cells: Characteristics, Microenvironment, and Therapy.Frontiers in pharmacology · 2016Review
Corrections and comments
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Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma multiforme (GBM) is the most common type of brain tumors with dismal outcomes. The mesenchymal phenotype is the hallmark of tumor aggressiveness in GBMs. Perivascular smooth muscle cells (pericytes) are essential in homeostasis of normal and glioma tissues. Here we found HMGA2, an architectural transcription factor that promotes mesenchymal phenotypes in a number of solid tumors, is highly expressed in mesenchymal subtype of GBMs and labels both glioma pericytes and glioma-initiating cells (GICs). Accordingly, depletion of HMGA2 in GICs resulted in compromised self-renewal and tumorigenic capability, as well as undermined mesenchymal or pericyte differentiation. We further showed HMGA2 allows expressions of FOXM1 and PLAU to maintain GIC propagation, gliomagenesis and aggressiveness both in vitro and in vivo. Therefore, suppressing HMGA2-mediated GIC self-renewal and invasiveness might be a promising means to treat GBMs.
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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.