rdf:type |
|
lifeskim:mentions |
umls-concept:C0043167,
umls-concept:C0065389,
umls-concept:C0086418,
umls-concept:C0178539,
umls-concept:C0334227,
umls-concept:C0600210,
umls-concept:C0682972,
umls-concept:C1140680,
umls-concept:C1269955,
umls-concept:C1314939,
umls-concept:C2699153
|
pubmed:issue |
23
|
pubmed:dateCreated |
2007-9-11
|
pubmed:abstractText |
We investigated whether lysophosphatidylethanolamine (LPE) modulates cellular signaling in different cell types. SK-OV3 ovarian cancer cells and OVCAR-3 ovarian cancer cells were responsive to LPE. LPE-stimulated intracellular calcium concentration ([Ca(2+)](i)) increase was inhibited by U-73122, suggesting that LPE stimulates calcium signaling via phospholipase C activation. Moreover, pertussis toxin (PTX) almost completely inhibited [Ca(2+)](i) increase by LPE, indicating the involvement of PTX-sensitive G-proteins. Furthermore, we found that LPE stimulated chemotactic migration and cellular invasion in SK-OV3 ovarian cancer cells. We examined the role of lysophosphatidic acid receptors on LPE-stimulated cellular responses using HepG2 cells transfected with different LPA receptors, and found that LPE failed to stimulate nuclear factor kappa B-driven luciferase. We suggest that LPE stimulates a membrane bound receptor, different from well known LPA receptors, resulting in chemotactic migration and cellular invasion in SK-OV3 ovarian cancer cells.
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pubmed:language |
eng
|
pubmed:journal |
|
pubmed:citationSubset |
IM
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/GTP-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Luciferases,
http://linkedlifedata.com/resource/pubmed/chemical/Lysophospholipids,
http://linkedlifedata.com/resource/pubmed/chemical/Pertussis Toxin,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, G-Protein-Coupled,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Lysophosphatidic Acid,
http://linkedlifedata.com/resource/pubmed/chemical/Recombinant Fusion Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Type C Phospholipases,
http://linkedlifedata.com/resource/pubmed/chemical/lysophosphatidylethanolamine
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
|
pubmed:issn |
0014-5793
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pubmed:author |
|
pubmed:issnType |
Print
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pubmed:day |
18
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pubmed:volume |
581
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pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
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pubmed:pagination |
4411-6
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pubmed:meshHeading |
pubmed-meshheading:17719584-Calcium,
pubmed-meshheading:17719584-Cell Line, Tumor,
pubmed-meshheading:17719584-Cell Movement,
pubmed-meshheading:17719584-Chemotaxis,
pubmed-meshheading:17719584-Dose-Response Relationship, Drug,
pubmed-meshheading:17719584-Female,
pubmed-meshheading:17719584-GTP-Binding Proteins,
pubmed-meshheading:17719584-Gene Expression Regulation, Neoplastic,
pubmed-meshheading:17719584-HeLa Cells,
pubmed-meshheading:17719584-Humans,
pubmed-meshheading:17719584-Luciferases,
pubmed-meshheading:17719584-Lysophospholipids,
pubmed-meshheading:17719584-Neoplasm Invasiveness,
pubmed-meshheading:17719584-Ovarian Neoplasms,
pubmed-meshheading:17719584-Pertussis Toxin,
pubmed-meshheading:17719584-RNA, Messenger,
pubmed-meshheading:17719584-Receptors, G-Protein-Coupled,
pubmed-meshheading:17719584-Receptors, Lysophosphatidic Acid,
pubmed-meshheading:17719584-Recombinant Fusion Proteins,
pubmed-meshheading:17719584-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:17719584-Transfection,
pubmed-meshheading:17719584-Type C Phospholipases,
pubmed-meshheading:17719584-U937 Cells
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pubmed:year |
2007
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pubmed:articleTitle |
Lysophosphatidylethanolamine stimulates chemotactic migration and cellular invasion in SK-OV3 human ovarian cancer cells: involvement of pertussis toxin-sensitive G-protein coupled receptor.
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pubmed:affiliation |
Department of Biochemistry, College of Medicine, Dong-A University, Busan 602-714, Republic of Korea.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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