國家衛生研究院 NHRI:Item 3990099045/2221
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    题名: Interleukin-6 acts as an antiapoptotic factor in human esophageal carcinoma cells through the activation of both STAT3 and mitogen-activated protein kinase pathways
    作者: Leu, CM;Wong, FH;Chang, CM;Huang, SF;Hu, CP
    贡献者: Division of Molecular and Genomic Medicine
    摘要: The production of interleukin-6 (IL-6) has been discovered in a variety of human tumors. Here we report the expression of IL-6, IL-6 receptor alpha (IL- 6Ralpha), and gp130 in human esophageal carcinoma tissues. We further demonstrate that IL- 6 protects an esophageal carcinoma cell line CE48T/VGH from apoptosis induced by staurosporine. IL-6 stimulation induced a rapid phosphorylation of gp130 and STAT3, and a dominant-negative STAT3 completely abolished the antiapoptotic effect. IL-6 also activated ERK 1/2 in CE48T/VGH cells. Inhibition of the ERK activation by PD98059 and transfection of a dominant-negative ERK2 completely blocked the protection of IL- 6 against apoptosis. Thus, both STAT and MAP kinase pathways are responsible for the IL-6-delivered survival signal in human esophageal carcinoma cells. In contrast, PI3-K inhibitors only partially attenuated the effect of IL-6, suggesting that PI3-K does not play a major role in the antiapoptotic signal of IL- 6 in our system. To investigate whether IL- 6 could induce the production of antiapoptotic molecules, proteins of the Bcl-2 family were measured. While Bcl-2, Bcl- x(L),, and Bax were not affected, Mcl-1 was induced by IL-6 in human esophageal carcinoma cells. Our results suggest that IL- 6 may contribute to the progression of esophageal cancers in an autocrine or paracrine manner.
    关键词: Biochemistry & Molecular Biology;Oncology;Cell Biology;Genetics & Heredity
    日期: 2003-10-30
    關聯: Oncogene. 2003 Oct;22(49):7809-7818.
    Link to: http://dx.doi.org/10.1038/sj.onc.1207084
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=0950-9232&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000186240200011
    Cited Times(Scopus): http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=0344441877
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