| Lack of FasL-mediated killing leads to in vivo tumor promotion in mouse Lewis lung cancer. | |
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MedLine Citation:
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PMID: 12766475 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Lewis lung carcinoma (3LL) cells were constitutively resistant to Fas-mediated apoptosis, but overexpression of Fas on 3LL cells allowed Fas-mediated apoptosis after crosslinking with agonist anti-Fas antibody (Jo2) in vitro. Surprisingly, Fas-overexpressing 3LL cells showed enhanced in vivo tumor progression, whereas no promotion of in vivo tumor growth was observed for dominant negative (DN) Fas-overexpressing 3LL transfectants in which the cytoplasmic death domain was deleted. In addition, the promotion of in vivo tumor growth by Fas-overexpression was reduced in gld (FasL-mutation) mice compared to normal mice. These data indicate that intact Fas/FasL cell signaling is required for the promotion of in vivo tumor growth by Fas overexpression in 3LL cells. In contrast to the efficient Fas-mediated killing induced in vitro by crosslinking with anti-Fas antibody, Fas-overexpressing 3LL cells were resistant in vitro to Fas-mediated apoptosis by activated T cells or transient FasL transfection. These data suggest that agonist anti-Fas antibody and natural FasL can transmit qualitatively different signals, and crosslinking of Fas with natural FasL on 3LL cells does not deliver the expected death signal. Thus, our results demonstrate that in some cases overexpression of Fas can result in a survival advantage for tumor cells in vivo. |
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Authors:
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J-K Lee; T J Sayers; T C Back; J M Wigginton; R H Wiltrout |
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Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: Apoptosis : an international journal on programmed cell death Volume: 8 ISSN: 1360-8185 ISO Abbreviation: Apoptosis Publication Date: 2003 Mar |
Date Detail:
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Created Date: 2003-05-26 Completed Date: 2004-01-08 Revised Date: 2008-11-21 |
Medline Journal Info:
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Nlm Unique ID: 9712129 Medline TA: Apoptosis Country: United States |
Other Details:
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Languages: eng Pagination: 151-60 Citation Subset: IM |
Affiliation:
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National Genome Research Institute, National Institute of Health, 5 Nokbun-dong, Eunpyung-ku, Seoul 122-701, Korea. cookie_jklee@hotmail.com |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Apoptosis* Carcinoma, Lewis Lung / pathology* Cell Division Cross-Linking Reagents / pharmacology Cytoplasm / metabolism DNA / metabolism Disease Progression Fas Ligand Protein Flow Cytometry Genetic Vectors Interferon-gamma / metabolism Membrane Glycoproteins / metabolism, physiology* Mice Mice, Inbred C57BL Mutation Neoplasms / pathology Protein Structure, Tertiary Signal Transduction T-Lymphocytes / metabolism Time Factors Transfection Up-Regulation |
| Chemical | |
Reg. No./Substance:
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0/Cross-Linking Reagents; 0/Fas Ligand Protein; 0/Fasl protein, mouse; 0/Membrane Glycoproteins; 82115-62-6/Interferon-gamma; 9007-49-2/DNA |
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