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dc.contributor.authorLiu, Zhongchenzh_CN
dc.contributor.authorWang, Juanzh_CN
dc.contributor.authorYin, Pingzh_CN
dc.contributor.authorQiu, Jinhuazh_CN
dc.contributor.authorLiu, Ruizhenzh_CN
dc.contributor.authorLi, Wenzhuzh_CN
dc.contributor.authorFan, Xinzh_CN
dc.contributor.authorCheng, Xiaofengzh_CN
dc.contributor.authorChen, Caixiazh_CN
dc.contributor.authorZhang, Jiakaizh_CN
dc.contributor.authorZhuang, Guohongzh_CN
dc.contributor.author王军zh_CN
dc.date.accessioned2013-12-12T02:08:30Z
dc.date.available2013-12-12T02:08:30Z
dc.date.issued2009-08zh_CN
dc.identifier.citationCellular & Molecular Immunology, 2009,6(4):285-293zh_CN
dc.identifier.issn1672-7681zh_CN
dc.identifier.otherISI:000274324000007zh_CN
dc.identifier.urihttps://dspace.xmu.edu.cn/handle/2288/60552
dc.descriptionNatural Science Foundation of Fujian Province [C0710046]zh_CN
dc.description.abstractDespite impressive results obtained in animal models, the clinical use of Fas ligand (FasL) as an anticancer drug is limited by severe toxicity. Systemic toxicity of death ligands may be prevented by using genes encoding membrane-bound death ligands and by targeted transgene expression through either targeted transduction or targeted transcription. Selective induction of tumor cell death is a promising anticancer strategy. A fusion protein is created by fusing the extracellular domain of Fas ligand (FasL) to the peptide arginine-glycine-aspartic acid (RGD) that selectively targets av beta 3-integrins on tumor endothelial cells. The purpose of this study is to evaluate the effects of RGD-FasL on tumor growth and survival in a murine hepatocellular carcinoma (HCC) tumor model. Treatment with RGD-FasL displaying an obvious suppressive effect on the HCC tumor model as compared to that with FasL (p < 0.05) and resulted in a more additive effect on tumor growth delay in this model. RGD-FasL treatment significantly enhanced mouse survival and caused no toxic effect, such as weight loss, organ failure, or other treatment-related toxicities. Apoptosis was detected by flow cytometric analysis and TUNEL assays; those results also showed that RGD-FasL is a more potent inducer of cell apoptosis for H22 and H9101 cell lines than FasL (p < 0.05). In conclusion, RGD-FasL appears to be a low-toxicity selective inducer of tumor cell death, which merits further investigation in preclinical and clinical studies. Furthermore, this approach offers a versatile technology for complexing target ligands with therapeutic recombinant proteins. To distinguish the anti-tumor effects of FasL in vivo, tumor and liver tissues were harvested to examine for evidence of necrotic cells, tumor cells, or apoptotic cells by Hematoxylin and eosin (H&E) staining. Cellular & Molecular Immunology. 2009;6(4):285-293.zh_CN
dc.language.isoen_USzh_CN
dc.subjectTUMOR-NECROSIS-FACTORzh_CN
dc.subjectGLY-ASP SEQUENCEzh_CN
dc.subjectFACTOR-ALPHAzh_CN
dc.subjectINTERFERON-GAMMAzh_CN
dc.subjectDRUG-DELIVERYzh_CN
dc.subjectEXPRESSIONzh_CN
dc.subjectMELPHALANzh_CN
dc.subjectPERFUSIONzh_CN
dc.subjectINTEGRINzh_CN
dc.subjectBINDINGzh_CN
dc.titleRGD-FasL Induces Apoptosis in Hepatocellular Carcinomazh_CN
dc.typeArticlezh_CN


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