| pubmed-article:16936263 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16936263 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
| pubmed-article:16936263 | lifeskim:mentions | umls-concept:C0597032 | lld:lifeskim |
| pubmed-article:16936263 | lifeskim:mentions | umls-concept:C0206698 | lld:lifeskim |
| pubmed-article:16936263 | lifeskim:mentions | umls-concept:C0014939 | lld:lifeskim |
| pubmed-article:16936263 | lifeskim:mentions | umls-concept:C0007595 | lld:lifeskim |
| pubmed-article:16936263 | lifeskim:mentions | umls-concept:C0021665 | lld:lifeskim |
| pubmed-article:16936263 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:16936263 | pubmed:dateCreated | 2006-8-28 | lld:pubmed |
| pubmed-article:16936263 | pubmed:abstractText | We investigated the expression of estrogen receptors (ERs), insulin-like growth factor 1 (IGF-1), and IGF-1R (receptor) in human cholangiocarcinoma and cholangiocarcinoma cell lines (HuH-28, TFK-1, Mz-ChA-1), evaluating the role of estrogens and IGF-1 in the modulation of neoplastic cell growth. ER-alpha, ER-beta, IGF-1, and IGF-1R were expressed (immunohistochemistry) in all biopsies (18 of 18) of intrahepatic cholangiocarcinoma. ER-alpha was expressed (Western blot) only by the HuH-28 cell line (intrahepatic cholangiocarcinoma), whereas ER-beta, IGF-1, and IGF-1R were expressed in the three cell lines examined. In serum-deprived HuH-28 cells, serum readmission induced stimulation of cell proliferation that was inhibited by ER and IGF-1R antagonists. 17beta-Estradiol and IGF-1 stimulated proliferation of HuH-28 cells to a similar extent to that of MCF7 (breast cancer) but greater than that of TFK-1 and Mz-ChA-1, inhibiting apoptosis and exerting additive effects. These effects of 17beta-estradiol and IGF-1 were associated with enhanced protein expression of ER-alpha, phosphorylated (p)-ERK1/2 and pAKT but with decreased expression of ER-beta. Finally, transfection of IGF-1R anti-sense oligonucleotides in HuH-28 cells markedly decreased cell proliferation. In conclusion, human intrahepatic cholangiocarcinomas express receptors for estrogens and IGF-1, which cooperate in the modulation of cell growth and apoptosis. Modulation of ER and IGF-1R could represent a strategy for the management of cholangiocarcinoma. | lld:pubmed |
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| pubmed-article:16936263 | pubmed:language | eng | lld:pubmed |
| pubmed-article:16936263 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16936263 | pubmed:citationSubset | AIM | lld:pubmed |
| pubmed-article:16936263 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:16936263 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16936263 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:16936263 | pubmed:issn | 0002-9440 | lld:pubmed |
| pubmed-article:16936263 | pubmed:author | pubmed-author:FHH | lld:pubmed |
| pubmed-article:16936263 | pubmed:author | pubmed-author:BenedettiAnto... | lld:pubmed |
| pubmed-article:16936263 | pubmed:author | pubmed-author:AlvaroDomenic... | lld:pubmed |
| pubmed-article:16936263 | pubmed:author | pubmed-author:MarucciLucaL | lld:pubmed |
| pubmed-article:16936263 | pubmed:author | pubmed-author:AlpiniGianfra... | lld:pubmed |
| pubmed-article:16936263 | pubmed:author | pubmed-author:AttiliAdolfo... | lld:pubmed |
| pubmed-article:16936263 | pubmed:author | pubmed-author:GaudioEugenio... | lld:pubmed |
| pubmed-article:16936263 | pubmed:author | pubmed-author:FrancisHeathe... | lld:pubmed |
| pubmed-article:16936263 | pubmed:author | pubmed-author:OnoriPaoloP | lld:pubmed |
| pubmed-article:16936263 | pubmed:author | pubmed-author:FranchittoAnt... | lld:pubmed |
| pubmed-article:16936263 | pubmed:author | pubmed-author:GlaserShannon... | lld:pubmed |
| pubmed-article:16936263 | pubmed:author | pubmed-author:SterpettiPaol... | lld:pubmed |
| pubmed-article:16936263 | pubmed:author | pubmed-author:De... | lld:pubmed |
| pubmed-article:16936263 | pubmed:author | pubmed-author:DostalDavid... | lld:pubmed |
| pubmed-article:16936263 | pubmed:author | pubmed-author:Onetti... | lld:pubmed |
| pubmed-article:16936263 | pubmed:author | pubmed-author:Ginanni-Corra... | lld:pubmed |
| pubmed-article:16936263 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:16936263 | pubmed:volume | 169 | lld:pubmed |
| pubmed-article:16936263 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16936263 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:16936263 | pubmed:pagination | 877-88 | lld:pubmed |
| pubmed-article:16936263 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
