ArticleCancer research2011
Nonredundant functions for Akt isoforms in astrocyte growth and gliomagenesis in an orthotopic transplantation model.
Article in Cancer research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 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.
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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
46 citing papers in PubMed, 61 citations in OpenAlex.
- Peptides from the Shadows: Molecular Depth Insights and Clinical Horizons of Circular RNA-encoded Peptides in Gliomas.Neuromolecular medicine · 2026Review
- Reactive Astrocytes in Glioma: Emerging Opportunities and Challenges.International journal of molecular sciences · 2025Review
- The anatomy of neuroepithelial tumours.Brain : a journal of neurology · 2023Article
- The Oncogenesis of Glial Cells in Diffuse Gliomas and Clinical Opportunities.Neuroscience bulletin · 2023Review
- Isoforms of autophagy-related proteins: role in glioma progression and therapy resistance.Molecular and cellular biochemistry · 2022Review
- Conventional Therapies Deplete Brain-Infiltrating Adaptive Immune Cells in a Mouse Model of Group 3 Medulloblastoma Implicating Myeloid Cells as Favorable Immunotherapy Targets.Frontiers in immunology · 2022Article
- Patient-derived models recapitulate heterogeneity of molecular signatures and drug response in pediatric high-grade glioma.Nature communications · 2021Article
- Small-molecule screen reveals synergy of cell cycle checkpoint kinase inhibitors with DNA-damaging chemotherapies in medulloblastoma.Science translational medicine · 2021Article
- Assessment of Cannabidiol and Δ9-Tetrahydrocannabiol in Mouse Models of Medulloblastoma and Ependymoma.Cancers · 2021Article
- Article
- Adaptive Molecular Evolution ofBioMed research international · 2020Article
- NT3Stem cell research & therapy · 2019Article
- A novel tumor suppressor protein encoded by circular AKT3 RNA inhibits glioblastoma tumorigenicity by competing with active phosphoinositide-dependent Kinase-1.Molecular cancer · 2019Article
- Developmental origins and oncogenic pathways in malignant brain tumors.Wiley interdisciplinary reviews. Developmental biology · 2019Review
- Isoform-Specific Role of Akt in Oral Squamous Cell Carcinoma.Biomolecules · 2019Article
- Research progress on the PI3K/AKT signaling pathway in gynecological cancer (Review).Molecular medicine reports · 2019Review
- Precision Revisited: Targeting Microcephaly Kinases in Brain Tumors.International journal of molecular sciences · 2019Review
- H3.3 K27M depletion increases differentiation and extends latency of diffuse intrinsic pontine glioma growth in vivo.Acta neuropathologica · 2019Article
- Astrocyte-Specific Deletion of Sox2 Promotes Functional Recovery After Traumatic Brain Injury.Cerebral cortex (New York, N.Y. : 1991) · 2019Article
- Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The AKT family, comprising three highly homologous kinases, is an essential mediator of the PTEN/PI3K pathway, which is deregulated in many human cancers. A thorough understanding of the specific activities of each isoform in normal and disease tissues is lacking. We evaluated the role of each Akt isoform in gliomagenesis by using a model system driven by common glioma abnormalities, loss of function of p53 and Pten, and expression of EGFRvIII. Both Pten deletion and EGFRvIII expression accelerated the proliferation of p53-null primary murine astrocytes. All three Akt isoforms were expressed and phosphorylated in astrocytes, with significantly higher activation in Pten-null cells. Despite substantial compensation in many contexts when individual Akt isoforms were inhibited, isoform-specific effects were also identified. Specifically, loss of Akt1 or Akt2 decreased proliferation of Pten wild-type astrocytes, whereas combined loss of multiple isoforms was needed to inhibit proliferation of Pten-null astrocytes. In addition, Akt3 was required for anchorage-independent growth of transformed astrocytes and human glioma cells, and Akt3 loss inhibited invasion of transformed astrocytes. EGFRvIII expression transformed p53-null astrocytes with or without Pten deletion, causing rapid development of high-grade astrocytoma on intracranial transplantation. Furthermore, tumorigenesis of Pten;p53-null astrocytes expressing EGFRvIII was delayed by Akt1 loss and accelerated by Akt2 loss. Taken together, these results indicate context-dependent roles for individual Akt isoforms and suggest that there may be heterogeneous tumor response to isoform-specific inhibitors.
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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.