ArticleScience signaling2014
Targeting aPKC disables oncogenic signaling by both the EGFR and the proinflammatory cytokine TNFα in glioblastoma.
Article in Science signaling, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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
32 citing papers in PubMed, 46 citations in OpenAlex.
- Cell polarity proteins promote macropinocytosis in response to metabolic stress.Nature communications · 2024Article
- Chemerin enhances mesenchymal features of glioblastoma by establishing autocrine and paracrine networks in a CMKLR1-dependent manner.Oncogene · 2022Article
- Macrophages-aPKCJournal of experimental & clinical cancer research : CR · 2022Article
- Small Molecule Inhibitors in Adult High-Grade Glioma: From the Past to the Future.Frontiers in oncology · 2022Review
- A Heterotypic Tridimensional Model to Study the Interaction of Macrophages and Glioblastoma In Vitro.International journal of molecular sciences · 2021Article
- Characterization of the m6A-Associated Tumor Immune Microenvironment in Prostate Cancer to Aid Immunotherapy.Frontiers in immunology · 2021Article
- Knockdown of IKKβ Inhibits Tumor Development in a Leptomeningeal Metastasis Mouse Model and Proliferation of Lung Cancer Cells.Cancer management and research · 2020Article
- The Dual Roles of the Atypical Protein Kinase Cs in Cancer.Cancer cell · 2019Review
- aPKC in neuronal differentiation, maturation and function.Neuronal signaling · 2019Review
- TNFα inhibitor C87 sensitizes EGFRvIII transfected glioblastoma cells to gefitinib by a concurrent blockade of TNFα signaling.Cancer biology & medicine · 2019Article
- Pard3 suppresses glioma invasion by regulating RhoA through atypical protein kinase C/NF-κB signaling.Cancer medicine · 2019Article
- Activation of atypical protein kinase C by sphingosine 1-phosphate revealed by an aPKC-specific activity reporter.Science signaling · 2019Article
- Junin Virus Triggers Macrophage Activation and Modulates Polarization According to Viral Strain Pathogenicity.Frontiers in immunology · 2019Article
- PAR3-PAR6-atypical PKC polarity complex proteins in neuronal polarization.Cellular and molecular life sciences : CMLS · 2018Review
- aPKCζ-dependent Repression of Yap is Necessary for Functional Restoration of Irradiated Salivary Glands with IGF-1.Scientific reports · 2018Article
- Article
- Protein kinase C: perfectly balanced.Critical reviews in biochemistry and molecular biology · 2018Review
- Protein kinase C as a tumor suppressor.Seminars in cancer biology · 2018Review
- Macrophages and Galectin 3 Control Bacterial Burden in Acute and Subacute Murine Leptospirosis That Determines Chronic Kidney Fibrosis.Frontiers in cellular and infection microbiology · 2018Article
- Tumor-derived fibulin-3 activates pro-invasive NF-κB signaling in glioblastoma cells and their microenvironment.Oncogene · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors at 8 institutions in 1 country.
Funding
Abstract
Grade IV glioblastoma is characterized by increased kinase activity of epidermal growth factor receptor (EGFR); however, EGFR kinase inhibitors have failed to improve survival in individuals with this cancer because resistance to these drugs often develops. We showed that tumor necrosis factor-α (TNFα) produced in the glioblastoma microenvironment activated atypical protein kinase C (aPKC), thereby producing resistance to EGFR kinase inhibitors. Additionally, we identified that aPKC was required both for paracrine TNFα-dependent activation of the transcription factor nuclear factor κB (NF-κB) and for tumor cell-intrinsic receptor tyrosine kinase signaling. Targeting aPKC decreased tumor growth in mouse models of glioblastoma, including models of EGFR kinase inhibitor-resistant glioblastoma. Furthermore, aPKC abundance and activity were increased in human glioblastoma tumor cells, and high aPKC abundance correlated with poor prognosis. Thus, targeting aPKC might provide an improved molecular approach for glioblastoma therapy.
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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.