國家衛生研究院 NHRI:Item 3990099045/11707
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    题名: Expression of FLJ10540, a novel oncogene, is associated with liver carcinogenesis and tumor progression through the activation of PKB/AKT pathway
    作者: Chen, CH;Huang, CYF;Lu, PJ;Chen, YC;Chou, CK
    贡献者: National Institute of Cancer Research
    摘要: The explosion of microarray study has promised to shed light on the identification of potential disease markers and drug targets. A significant challenge is how to prioritize those differentially expressed and uncharacterized novel genes in tumor tissues. One such category is cell cycle regulated genes that are only evolved in higher organisms but not in lower eukaryotic cells. Characterization of these genes may reveal some novel human cancer specific abnormalities. Of the novel targets identified, FLJ10540 is overexpressed in human hepatocellular carcinoma (HCC) as examined by quantitative RT-PCR and immuno-histochemistry. FLJ10540 is highly expressed in various adult normal tissues including the placenta, thymus, ovary, small intestine and pancreas, but not in normal liver. By using overexpression of FLJ10540 or knock down with FLJ10540 siRNA approaches, we conclude that FLJ10540 displays several characteristics of oncogene, including enhance cell growth at low serum levels, confer drug resistance, exhibit anchorage-independent growth, and induce rapid tumorigenesis in nude mice. Finally, FLJ10540 overexpression stimulates phosphatidylinositol (PI) 3-kinase activity, leading to increased phosphorylation levels of Akt and its downstream targets. FLJ10540-elicited cell transformation can be inhibited by a PI3-kinase inhibitor (Wortmannin). Taken together, these results strongly suggest that FLJ10540 is a potential novel oncogene that may play a role in the carcinogenesis of human cancer cells.
    日期: 2006-04
    關聯: Cancer Research. 2006 Apr;66(8, Suppl.):610.
    Link to: http://cancerres.aacrjournals.org/content/66/8_Supplement/610.4
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=0008-5472&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000454606200560
    显示于类别:[黃奇英(2005-2007)] 會議論文/會議摘要

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