ArticleJournal of cancer research and clinical oncology1997
Increased phospholipase D activity in human breast cancer.
Article in Journal of cancer research and clinical oncology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 84 citations in OpenAlex.
- Metabolic basis of cardiac dysfunction in cancer patients.Current opinion in cardiology · 2024Review
- Role of miRNA-145, 148, and 185 and Stem Cells in Prostate Cancer.International journal of molecular sciences · 2022Review
- Phosphatidylcholine-Derived Lipid Mediators: The Crosstalk Between Cancer Cells and Immune Cells.Frontiers in immunology · 2022Review
- MicroRNA miR-145-5p inhibits Phospholipase D 5 (PLD5) to downregulate cell proliferation and metastasis to mitigate prostate cancer.Bioengineered · 2021Article
- Phospholipase Signaling in Breast Cancer.Advances in experimental medicine and biology · 2021Review
- Inhibition of phospholipase D2 augments histone deacetylase inhibitor-induced cell death in breast cancer cells.Biological research · 2020Article
- Mammalian phospholipase D: Function, and therapeutics.Progress in lipid research · 2020Review
- Phospholipase D2 in prostate cancer: protein expression changes with Gleason score.British journal of cancer · 2019Article
- Role of phospholipase D in migration and invasion induced by linoleic acid in breast cancer cells.Molecular and cellular biochemistry · 2019Article
- How miRs and mRNA deadenylases could post-transcriptionally regulate expression of tumor-promoting protein PLD.Advances in biological regulation · 2018Review
- Phospholipase D inhibitors reduce human prostate cancer cell proliferation and colony formation.British journal of cancer · 2018Article
- Targeting phospholipase D in cancer, infection and neurodegenerative disorders.Nature reviews. Drug discovery · 2017Review
- Down-regulation of MicroRNAs (MiRs) 203, 887, 3619 and 182 Prevents Vimentin-triggered, Phospholipase D (PLD)-mediated Cancer Cell Invasion.The Journal of biological chemistry · 2016Article
- Article
- Phospholipase D signaling pathways and phosphatidic acid as therapeutic targets in cancer.Pharmacological reviews · 2014Review
- Chemical modulation of glycerolipid signaling and metabolic pathways.Biochimica et biophysica acta · 2014Review
- Hyperactivation of EGFR and downstream effector phospholipase D1 by oncogenic FAM83B.Oncogene · 2014Article
- Increased cell growth due to a new lipase-GEF (Phospholipase D2) fastly acting on Ras.Cellular signalling · 2013Article
- Role of the autotaxin-lysophosphatidate axis in cancer resistance to chemotherapy and radiotherapy.Biochimica et biophysica acta · 2013Review
- Sustained activation of protein kinase C induces delayed phosphorylation and regulates the fate of epidermal growth factor receptor.PloS one · 2013Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Phospholipase D is believed to play an important role in cell proliferation and tumorigenesis. One of its major functions is to cause a sustained activation of protein kinase C through the primary production of phosphatidic acid from phosphatidylcholine by the enzyme, followed by dephosphorylation forming diacylglycerol. Protein kinase C is known to be activated or translocated in some tumors including breast tumors. In order to examine phospholipase D activity in breast tumors, surgical specimens of human breast tumors were obtained by mastectomy or wide excision, and their phospholipase D activities were assayed by determining the formation of phosphatidylethanol from phosphatidylcholine and ethanol. Phospholipase D activity was predominantly localized in the microsomal fraction of the tumor tissue and markedly stimulated by oleic acid. We observed a significant increase in phospholipase D activity in 17 out of 19 spontaneous human breast tumors as compared to adjacent histologically normal breast tissue. The mean specific activity in the tumors was 52.9 +/- 41.8 (SD) pmol min-1 mg protein-1 whereas the value for the normal breast tissue was 34.0 +/- 36.2 (SD) pmol min-1 mg protein-1 (P < 0.01; paired Wilcoxon's rank-sum test). The mean tumor/normal activity ratio was 2.37. Among prognostic factors, the nuclear grade, evaluated according to Schnitt et al., was found to be correlated with the activity ratio. Our results suggest a role for phospholipase D in human breast tumors. An elevation in phospholipase D activity is useful as a potential marker for malignant disease in the breast.
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