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dc.contributor.authorHan, Jiahuai
dc.contributor.author韩家淮
dc.contributor.authorRen, Jian-Lin
dc.contributor.authorPan, Jin-Shui
dc.contributor.authorLu, Ya-Pi
dc.contributor.authorSun, Peiqing(Scripps Res Inst)
dc.date.accessioned2011-07-30T03:34:56Z
dc.date.available2011-07-30T03:34:56Z
dc.date.issued2009
dc.identifier.citationCellular Signalling,Volume 21, Issue 3, March 2009, Pages 378-383zh_CN
dc.identifier.issn0898-6568
dc.identifier.urihttp://dx.doi.org/doi:10.1016/j.cellsig.2008.10.011
dc.identifier.urihttps://dspace.xmu.edu.cn/handle/2288/10296
dc.description.abstractInflammation acts as a double-edged sword in the pathogenesis of cancer. Inflammatory responses play a key role in eliminating potentially cancerous cells; however, an inflammatory microenvironment also promotes the development of cancer. Proinflammatory cytokines, the key mediators of inflammation, also play a dual role in oncogenesis. While they can promote neoplastic progression, recent studies have revealed an unexpected function of the inflammatory pathways in inhibiting cancer development. These studies demonstrate that cells undergoing senescence, a cellular program serving as a barrier to cancer development, produce increased amount of inflammatory cytokines. These inflammatory cytokines play an essential role in the initiation and maintenance of cellular senescence, and are responsible for triggering an innate immune response that clears the senescent tumor cells in vivo. The purpose of the present review is to discuss the dual roles of the inflammatory cytokines produced by senescent cells in the pathogenesis of cancer, and the signaling pathway mediating their role in cellular senescence. (c) 2008 Elsevier Inc. All rights reserved.zh_CN
dc.description.sponsorshipNational Basic Research Program of China [2009CB522200]zh_CN
dc.language.isoenzh_CN
dc.publisherELSEVIER SCIENCE INCzh_CN
dc.subjectInflammationzh_CN
dc.subjectSenescencezh_CN
dc.subjectCancerzh_CN
dc.titleInflammatory signaling and cellular senescencezh_CN
dc.typeArticlezh_CN


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