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rdf:type |
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lifeskim:mentions |
umls-concept:C0033414,
umls-concept:C0086418,
umls-concept:C0109317,
umls-concept:C0162638,
umls-concept:C0334227,
umls-concept:C0752312,
umls-concept:C1140680,
umls-concept:C1150579,
umls-concept:C1150587,
umls-concept:C1333340,
umls-concept:C1366882,
umls-concept:C1367731,
umls-concept:C1370600,
umls-concept:C1704259,
umls-concept:C1705632,
umls-concept:C1705767,
umls-concept:C1705791,
umls-concept:C1705987,
umls-concept:C2675903
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pubmed:issue |
3
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pubmed:dateCreated |
2006-7-25
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pubmed:abstractText |
Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) induces apoptosis in a variety of tumor cell lines but not typically in normal or nontransformed cells, which makes TRAIL a desirable therapeutic agent to fight cancer. Human phosphatidylethanolamine-binding protein 4 (hPEBP4) is a recently identified anti-apoptotic molecule and has been shown to be highly expressed in breast and ovarian cancer cells. We demonstrate that silencing of hPEBP4 in CaoV-3 ovarian cancer cells potentiates TRAIL-induced apoptosis. We found that endogenous hPEBP4 interacts with Raf-1 and MEK1 in TRAIL-treated CaoV-3 cells by co-immunoprecipitation analysis. Simultaneously, silencing of hPEBP4 in CaoV-3 cells enhances TRAIL-induced ERK and JNK activation. Moreover, the inhibitors of MEK1 or JNK can reduce hPEBP4-silence-induced TRAIL sensitivity. Therefore, silencing of hPEBP4 in CaoV-3 ovarian cancer promotes TRAIL-induced apoptosis, and the increased MAPK activation is required for the apoptosis sensitization. All these data indicate that silencing of hPEBP4, an important potential target, may be a promising approach for the treatment of ovarian cancer.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Apoptosis Regulatory Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/DNA-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Extracellular Signal-Regulated MAP...,
http://linkedlifedata.com/resource/pubmed/chemical/MAP Kinase Kinase 1,
http://linkedlifedata.com/resource/pubmed/chemical/MAP Kinase Kinase 4,
http://linkedlifedata.com/resource/pubmed/chemical/MAP2K1 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Glycoproteins,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-raf,
http://linkedlifedata.com/resource/pubmed/chemical/TNF-Related Apoptosis-Inducing...,
http://linkedlifedata.com/resource/pubmed/chemical/TNFSF10 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factors,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha,
http://linkedlifedata.com/resource/pubmed/chemical/enhancer-binding protein AP-4
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
1107-3756
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
18
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
505-10
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:16865237-Apoptosis,
pubmed-meshheading:16865237-Apoptosis Regulatory Proteins,
pubmed-meshheading:16865237-DNA-Binding Proteins,
pubmed-meshheading:16865237-Extracellular Signal-Regulated MAP Kinases,
pubmed-meshheading:16865237-Female,
pubmed-meshheading:16865237-Gene Expression,
pubmed-meshheading:16865237-Humans,
pubmed-meshheading:16865237-MAP Kinase Kinase 1,
pubmed-meshheading:16865237-MAP Kinase Kinase 4,
pubmed-meshheading:16865237-Membrane Glycoproteins,
pubmed-meshheading:16865237-Ovarian Neoplasms,
pubmed-meshheading:16865237-Protein Binding,
pubmed-meshheading:16865237-Proto-Oncogene Proteins c-raf,
pubmed-meshheading:16865237-RNA Interference,
pubmed-meshheading:16865237-Signal Transduction,
pubmed-meshheading:16865237-TNF-Related Apoptosis-Inducing Ligand,
pubmed-meshheading:16865237-Transcription Factors,
pubmed-meshheading:16865237-Tumor Cells, Cultured,
pubmed-meshheading:16865237-Tumor Necrosis Factor-alpha
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pubmed:year |
2006
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pubmed:articleTitle |
Anti-apoptotic hPEBP4 silencing promotes TRAIL-induced apoptosis of human ovarian cancer cells by activating ERK and JNK pathways.
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pubmed:affiliation |
Department of Obstetrics and Gynecology, Qilu Hospital of Shandong University, Shandong, Jinan 250012, P.R. China.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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