Source:http://linkedlifedata.com/resource/pubmed/id/17943530
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
2008-3-19
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pubmed:abstractText |
The majority of human endometrial, ovarian and breast cancers express receptors for gonadotropin-releasing hormone (GnRH). Their proliferation is time- and dose-dependently reduced by GnRH and its agonistic analogs. GnRH agonists inhibit the mitogenic signal transduction of growth factor receptors via activation of a phosphotyrosine phosphatase, resulting in downregulation of cancer cell proliferation. Induction of apoptosis is not involved. Recently we showed that the GnRH agonist triptorelin induces activation of nuclear factor-kappaB (NFkappaB) and thus reduces the apoptosis induced by the cytotoxic agent doxorubicin in human endometrial and ovarian cancer cells. The triptorelin-induced reduction of doxorubicin-induced apoptosis was blocked by inhibition of NFkappaB translocation into the nucleus. The present study was conducted to investigate whether knock-down of GnRH receptor expression reduces GnRH agonist-induced anti-apoptotic action. We show that knock-down of GnRH receptor expression results in an increase of doxorubicin-induced apoptosis in human endometrial and ovarian cancers and in the human breast cancer cell line MCF-7. These data further demonstrate that GnRH agonists suppress chemotherapeutic drug-induced apoptosis via activation of the GnRH receptor in these cancers. The situation is different with T-47-D breast cancer cells. After knock-down of GnRH receptor expression doxorubicin-induced apoptosis was decreased, indicating that GnRH agonists do not suppress chemotherapeutic drug-induced apoptosis in T-47-D breast cancer cells.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antibiotics, Antineoplastic,
http://linkedlifedata.com/resource/pubmed/chemical/Doxorubicin,
http://linkedlifedata.com/resource/pubmed/chemical/Gonadotropin-Releasing Hormone,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, LHRH,
http://linkedlifedata.com/resource/pubmed/chemical/Triptorelin Pamoate
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
0951-3590
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
24
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
24-9
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:17943530-Antibiotics, Antineoplastic,
pubmed-meshheading:17943530-Antineoplastic Combined Chemotherapy Protocols,
pubmed-meshheading:17943530-Apoptosis,
pubmed-meshheading:17943530-Breast Neoplasms,
pubmed-meshheading:17943530-Cell Line, Tumor,
pubmed-meshheading:17943530-Doxorubicin,
pubmed-meshheading:17943530-Drug Antagonism,
pubmed-meshheading:17943530-Endometrial Neoplasms,
pubmed-meshheading:17943530-Female,
pubmed-meshheading:17943530-Gonadotropin-Releasing Hormone,
pubmed-meshheading:17943530-Humans,
pubmed-meshheading:17943530-Ovarian Neoplasms,
pubmed-meshheading:17943530-Receptors, LHRH,
pubmed-meshheading:17943530-Triptorelin Pamoate
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pubmed:year |
2008
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pubmed:articleTitle |
Increase of doxorubicin-induced apoptosis after knock-down of gonadotropin-releasing hormone receptor expression in human endometrial, ovarian and breast cancer cells.
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pubmed:affiliation |
Department of Gynecology and Obstetrics, Georg-August-University, Göttingen, Germany.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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