ArticleCancer letters2007
Phospholipase D provides a survival signal in human cancer cells with activated H-Ras or K-Ras.
Article in Cancer letters, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 68 citations in OpenAlex.
- The Role of KRAS in Non-Small Cell Lung Cancer: From Molecular Background to Precision Medicine.International journal of molecular sciences · 2026Review
- The p53/ZEB1-PLD3 feedback loop regulates cell proliferation in breast cancer.Cell death & disease · 2023Article
- Phospholipase Family Enzymes in Lung Cancer: Looking for Novel Therapeutic Approaches.Cancers · 2023Review
- Synthetic Vulnerabilities in the KRAS Pathway.Cancers · 2022Review
- NRG1 fusion-driven tumors: biology, detection, and the therapeutic role of afatinib and other ErbB-targeting agents.Annals of oncology : official journal of the European Society for Medical Oncology · 2020Review
- Mammalian phospholipase D: Function, and therapeutics.Progress in lipid research · 2020Review
- Phospholipase D-dependent mTOR complex 1 (mTORC1) activation by glutamine.The Journal of biological chemistry · 2018Article
- Elevated phospholipase D activity in androgen-insensitive prostate cancer cells promotes both survival and metastatic phenotypes.Cancer letters · 2018Article
- Therapeutic potential of a phospholipase D1 inhibitory peptide fused with a cell-penetrating peptide as a novel anti-asthmatic drug in a Der f 2-induced airway inflammation model.Experimental & molecular medicine · 2018Article
- Comparative Network Analysis of Patients with Non-Small Cell Lung Cancer and Smokers for Representing Potential Therapeutic Targets.Scientific reports · 2017Article
- Membrane-binding and activation of LKB1 by phosphatidic acid is essential for development and tumour suppression.Nature communications · 2017Article
- A feedback mechanism between PLD and deadenylase PARN for the shortening of eukaryotic poly(A) mRNA tails that is deregulated in cancer cells.Biology open · 2017Article
- Integrative analysis of extracellular and intracellular bladder cancer cell line proteome with transcriptome: improving coverage and validity of -omics findings.Scientific reports · 2016Article
- Reciprocal regulation of AMP-activated protein kinase and phospholipase D.The Journal of biological chemistry · 2015Article
- Phospholipase D activates HIF-1-VEGF pathway via phosphatidic acid.Experimental & molecular medicine · 2014Article
- Phospholipase D signaling pathways and phosphatidic acid as therapeutic targets in cancer.Pharmacological reviews · 2014Review
- Phospholipase D in cell signaling: from a myriad of cell functions to cancer growth and metastasis.The Journal of biological chemistry · 2014Review
- Phospholipase D and the maintenance of phosphatidic acid levels for regulation of mammalian target of rapamycin (mTOR).The Journal of biological chemistry · 2014Review
- Hyperactivation of EGFR and downstream effector phospholipase D1 by oncogenic FAM83B.Oncogene · 2014Article
- Temporal production of the signaling lipid phosphatidic acid by phospholipase D2 determines the output of extracellular signal-regulated kinase signaling in cancer cells.Molecular and cellular biology · 2014Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Phospholipase D (PLD) is elevated in rodent fibroblasts expressing activated H-Ras mutants. We therefore examined the PLD activity in human cancer cells with activating Ras mutations. T24 bladder carcinoma cells express an activated H-Ras gene and Calu-1 lung carcinoma cells express an activated K-Ras gene. We report here that both of these cancer cell lines express highly elevated levels of PLD activity and that the PLD activity is dependent upon Ras. We also show that the PLD activity is dependent upon the Ras effector molecules RalA and phosphatidylinositol-3-kinase (PI3K). PLD activity has been shown to provide a survival signal in breast cancer cell lines that suppressed stress-induced apoptosis. Suppression of PLD activity in the T24 and Calu-1 cells resulted in apoptotic cell death in the absence of serum, indicating that the elevated PLD activity provided a survival signal in these cancer cell lines. Suppression of Ras, RalA, or PI3K also led to apoptosis in the absence of serum. These data indicate that a critical component of Ras signaling in human cancer cells is the activation of PLD and that targeting PLD survival signals in cancer cells could be an effective strategy to induce apoptosis in human cancers with activating Ras mutations.
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