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dc.contributor.authorMao, Yubin
dc.contributor.authorSong, Gang
dc.contributor.authorMing, Yanlin
dc.contributor.authorBao, Shiden
dc.contributor.author鲍仕登
dc.contributor.authorOuyang, Gaoliang
dc.contributor.author欧阳高亮
dc.date.accessioned2011-07-31T01:48:47Z
dc.date.available2011-07-31T01:48:47Z
dc.date.issued2008
dc.identifier.citationExp. Biol. Med. Song et al. 233 (12):1537-1545zh_CN
dc.identifier.issn1535-3702
dc.identifier.urihttp://dx.doi.org/doi:10.3181/0805-RM-164
dc.identifier.urihttps://dspace.xmu.edu.cn/handle/2288/10324
dc.description.abstractOsteopontin (OPN) is a secreted, integrin-binding matrix phosphorylated glycoprotein that is overexpressed in many advanced cancers. However, the functional mechanisms by which OPN contributes to gastric cancer development are poorly understood. Here, we report that curcumin inhibited the growth of SGC7901 cell and induced apoptosis in a concentration- and time-dependent manner, while the acquired expression of OPN in SGC7901 cells dramatically promoted cell survival under serum depletion and prevented curcumin-induced apoptosis. Furthermore, PI3-K inhibitor LY294002 attenuated OPN-mediated Akt activation. Moreover, inhibiting the binding of OPN to alpha(v)beta(3) integrins reduced activation of Akt. Taken together, these results demonstrate that the pro-survival and anti-apoptosis activities of OPN in gastric cancer cells are mediated in part through PI3-K/Akt pathway via alpha(v)beta(3) integrins. Exp Biol Med 233: 1537-1545, 2008zh_CN
dc.description.sponsorshipNational Natural science Foundation of China [30370307, 30400239, 30570915]; Program for New Century Excellent Talents in Xiamen Universityzh_CN
dc.language.isoenzh_CN
dc.publisherSOC EXPERIMENTAL BIOLOGY MEDICINEzh_CN
dc.subjectosteopontin (OPN)zh_CN
dc.subjectcurcuminzh_CN
dc.subjectapoptosiszh_CN
dc.subjectAktzh_CN
dc.subjectgastric cancerzh_CN
dc.titleOsteopontin Prevents Curcumin-Induced Apoptosis and Promotes Survival Through Akt Activation via alpha(v)beta(3) Integrins in Human Gastric Cancer Cellszh_CN
dc.typeArticlezh_CN


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