ArticleOncogene2008
The PEA-15/PED protein protects glioblastoma cells from glucose deprivation-induced apoptosis via the ERK/MAP kinase pathway.
Article in Oncogene, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.
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Who cites it
40 citing papers in PubMed, 1 synthesis or guideline pooled it, 60 citations in OpenAlex.
- Effect of ouabain on calcium signaling in rodent brain: A systematic review ofFrontiers in pharmacology · 2022Pooled it
- A system-wide investigation into the phosphoregulatory network of TNIK and its cellular implications.Frontiers in bioinformatics · 2026Article
- TMEM158 promotes ICC metastasis via inducing lactic acid mediated reduction of actin skeleton stiffness of ICC cells.Journal of advanced research · 2026Article
- PEA15 promotes osteosarcoma progression and cisplatin resistance by modulating autophagy through the FABP3-TNF signaling axis.iScience · 2025Article
- Transcriptome analysis of serum biomarker, shared gene signature and pharmacological targets between diabetic cardiomyopathy and nephropathy.Biochemistry and biophysics reports · 2025Article
- Proteomic Analysis of the Low Molecular Mass Fraction of Newly Diagnosed and Recurrent Glioblastoma CUSA Fluid: A Pilot Investigation of the Peptidomic Profile.International journal of molecular sciences · 2025Article
- Cell death in glioblastoma and the central nervous system.Cellular oncology (Dordrecht, Netherlands) · 2025Review
- Astrocytes-Derived Small Extracellular Vesicles Hinder Glioma Growth.Biomedicines · 2022Article
- Hemin-Induced Death Models Hemorrhagic Stroke and Is a Variant of Classical Neuronal Ferroptosis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Methodological Approaches for Assessing Metabolomic Changes in Glioblastomas.Methods in molecular biology (Clifton, N.J.) · 2022Review
- Proteomics analysis identifies PEA-15 as an endosomal phosphoprotein that regulates α5β1 integrin endocytosis.Scientific reports · 2021Article
- Overcoming TRAIL Resistance for Glioblastoma Treatment.Biomolecules · 2021Review
- Article
- MOB1A regulates glucose deprivation-induced autophagy via IL6-STAT3 pathway in gallbladder carcinoma.American journal of cancer research · 2020Article
- Sirtuin 7 promotes glioma proliferation and invasion through activation of the ERK/STAT3 signaling pathway.Oncology letters · 2019Article
- PEA15 promotes liver metastasis of colorectal cancer by upregulating the ERK/MAPK signaling pathway.Oncology reports · 2019Article
- Characterization of brain tumor initiating cells isolated from an animal model of CNS primitive neuroectodermal tumors.Oncotarget · 2018Article
- Role of JMJD2B in colon cancer cell survival under glucose-deprived conditions and the underlying mechanisms.Oncogene · 2018Article
- Kinomic profiling of glioblastoma cells reveals PLCG1 as a target in restricted glucose.Biomarker research · 2018Article
- Presenilin1/γ-secretase protects neurons from glucose deprivation-induced death by regulating miR-212 and PEA15.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
PEA-15 (phosphoprotein enriched in astrocytes 15 kDa) is a death effector domain-containing protein, which is involved in the regulation of apoptotic cell death. Since PEA-15 is highly expressed in cells of glial origin, we studied the role of PEA-15 in human malignant brain tumors. Immunohistochemical analysis of PEA-15 expression shows strong immunoreactivity in astrocytomas and glioblastomas. Phosphorylation of PEA-15 at Ser(116) is found in vivo in perinecrotic areas in glioblastomas and in vitro after glucose deprivation of glioblastoma cells. Overexpression of PEA-15 induces a marked resistance against glucose deprivation-induced apoptosis, whereas small interfering RNA (siRNA)-mediated downregulation of endogenous PEA-15 results in the sensitization to glucose withdrawal-mediated cell death. This antiapoptotic activity of PEA-15 under low glucose conditions depends on its phosphorylation at Ser(116). Moreover, siRNA-mediated knockdown of PEA-15 abolishes the tumorigenicity of U87MG glioblastoma cells in vivo. PEA-15 regulates the level of phosphorylated extracellular-regulated kinase (ERK)1/2 in glioblastoma cells and the PEA-15-dependent protection from glucose deprivation-induced cell death requires ERK1/2 signaling. PEA-15 transcriptionally upregulates the Glucose Transporter 3, which is abrogated by the inhibition of ERK1/2 phosphorylation. Taken together, our findings suggest that Ser(116)-phosphorylated PEA-15 renders glioma cells resistant to glucose deprivation-mediated cell death as encountered in poor microenvironments, for example in perinecrotic areas of glioblastomas.
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