ArticleThe Journal of biological chemistry2014
Phospholipase D2 mediates survival signaling through direct regulation of Akt in glioblastoma cells.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.
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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, 1 synthesis or guideline pooled it, 79 citations in OpenAlex.
- Sphingosine 1-phosphate (S1P) signaling in glioblastoma multiforme-A systematic review.International journal of molecular sciences · 2017Pooled it
- Neutrophil membrane-coated nanoparticles for targeted therapy.Discover nano · 2025Review
- Hispidulin: a potential alternative to vorinostat against HDAC1 for acute myeloid leukemia.Discover oncology · 2025Article
- Phosphatidic acid is involved in regulation of autophagy in neurons in vitro and in vivo.Pflugers Archiv : European journal of physiology · 2024Article
- PLD1 is a key player in cancer stemness and chemoresistance: Therapeutic targeting of cross-talk between the PI3K/Akt and Wnt/β-catenin pathways.Experimental & molecular medicine · 2024Review
- Phospholipases in Gliomas: Current Knowledge and Future Perspectives from Bench to Bedside.Biomolecules · 2023Review
- Modified 5-aminolevulinic acid photodynamic therapy suppresses cutaneous squamous cell carcinoma through blocking Akt/mTOR-mediated autophagic flux.Frontiers in pharmacology · 2023Article
- Lipid Alterations in Glioma: A Systematic Review.Metabolites · 2022Review
- Phospholipase D2 is a positive regulator of sirtuin 1 and modulates p53-mediated apoptosis via sirtuin 1.Experimental & molecular medicine · 2021Article
- mTOR-Rictor-EGFR axis in oncogenesis and diagnosis of glioblastoma multiforme.Molecular biology reports · 2021Review
- Structure and regulation of human phospholipase D.Advances in biological regulation · 2021Review
- Phospholipase D1 is upregulated by vorinostat and confers resistance to vorinostat in glioblastoma.Journal of cellular physiology · 2021Article
- Phospholipase D1 inhibition sensitizes glioblastoma to temozolomide and suppresses its tumorigenicity.The Journal of pathology · 2020Article
- Increased phospholipase D activity contributes to tumorigenesis in prostate cancer cell models.Molecular and cellular biochemistry · 2020Article
- Phospholipase D1 and D2 Synergistically Regulate Thrombus Formation.International journal of molecular sciences · 2020Article
- New Era of Diacylglycerol Kinase, Phosphatidic Acid and Phosphatidic Acid-Binding Protein.International journal of molecular sciences · 2020Review
- Mammalian phospholipase D: Function, and therapeutics.Progress in lipid research · 2020Review
- Treatment with Gold Nanoparticles UsingInternational journal of molecular sciences · 2020Article
- High Expression of PhospholipaseD2 Induced by Hypoxia Promotes Proliferation of Colon Cancer Cells through Activating NF- κ Bp65 Signaling Pathway.Pathology oncology research : POR · 2020Article
- Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The lack of innovative drug targets for glioblastoma multiforme (GBM) limits patient survival to approximately 1 year following diagnosis. The pro-survival kinase Akt provides an ideal target for the treatment of GBM as Akt signaling is frequently activated in this cancer type. However, the central role of Akt in physiological processes limits its potential as a therapeutic target. In this report, we show that the lipid-metabolizing enzyme phospholipaseD(PLD) is a novel regulator of Akt inGBM.Studies using a combination of small molecule PLD inhibitors and siRNA knockdowns establish phosphatidic acid, the product of the PLD reaction, as an essential component for the membrane recruitment and activation of Akt. Inhibition of PLD enzymatic activity and subsequent Akt activation decreases GBM cell viability by specifically inhibiting autophagic flux. We propose a mechanism whereby phosphorylation of beclin1 by Akt prevents binding of Rubicon (RUN domain cysteine-rich domain containing beclin1-interacting protein), an interaction known to inhibit autophagic flux. These findings provide a novel framework through which Akt inhibition can be achieved without directly targeting the kinase.
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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.