ArticleCell cycle (Georgetown, Tex.)2012
Choline-releasing glycerophosphodiesterase EDI3 links the tumor metabolome to signaling network activities.
Article in Cell cycle (Georgetown, Tex.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 34 citations in OpenAlex.
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- Nuclear magnetic resonance-based tissue metabolomic analysis clarifies molecular mechanisms of gastric carcinogenesis.Cancer science · 2020Article
- Untargeted LC-HRMS-based metabolomics to identify novel biomarkers of metastatic colorectal cancer.Scientific reports · 2019Article
- The glycerophosphocholine acyltransferase Gpc1 is part of a phosphatidylcholine (PC)-remodeling pathway that alters PC species in yeast.The Journal of biological chemistry · 2019Article
- Highlight report: Role of choline phospholipid metabolism in tumor progression.EXCLI journal · 2019Article
- Highlight report: Tumor infiltrating lymphocytes in breast cancer.EXCLI journal · 2019Article
- Lysophosphatidic acid in carcinogenesis and tumor development.EXCLI journal · 2018Article
- Identification and causes of metabonomic difference between orthotopic and subcutaneous xenograft of pancreatic cancer.Oncotarget · 2017Article
- Integrins and Cell Metabolism: An Intimate Relationship Impacting Cancer.International journal of molecular sciences · 2017Review
- Dysregulated choline metabolism in T-cell lymphoma: role of choline kinase-α and therapeutic targeting.Blood cancer journal · 2015Article
- Highlights in tumor metabolome research: Choline metabolism influences integrin expression and supports cell attachment.EXCLI journal · 2014Article
- EDI3 links choline metabolism to integrin expression, cell adhesion and spreading.Cell adhesion & migration · 2014Article
- Article
- Hippocampal and thalamic neuronal metabolism in a putative rat model of schizophrenia.Neural regeneration research · 2013Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recently, EDI3 was identified as a key factor for choline metabolism that controls tumor cell migration and is associated with metastasis in endometrial carcinomas. EDI3 cleaves glycerophosphocholine (GPC) to form choline and glycerol-3-phosphate (G3P). Choline is then further metabolized to phosphatidylcholine (PtdC), the major lipid in membranes and a key player in membrane-mediated cell signaling. The second product, G3P, is a precursor molecule for several lipids with central roles in signaling, for example lysophosphatidic acid (LPA), phosphatidic acid (PA) and diacylglycerol (DAG). LPA activates intracellular signaling pathways by binding to specific LPA receptors, including membrane-bound G protein-coupled receptors and the intracellular nuclear receptor, PPARγ. Conversely, PA and DAG mediate signaling by acting as lipid anchors that bind and activate several signaling proteins. For example, binding of GTPases and PKC to PA and DAG, respectively, increases the activation of signaling networks, mediating processes such as migration, adhesion, proliferation or anti-apoptosis-all relevant for tumor development. We present a concept by which EDI3 either directly generates signaling molecules or provides "membrane anchors" for downstream signaling factors. As a result, EDI3 links choline metabolism to signaling activities resulting in a more malignant phenotype.
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