Fascaplysin sensitizes cells to TRAIL-induced apoptosis through upregulating DR5 expression
Identifieur interne : 002143 ( Main/Exploration ); précédent : 002142; suivant : 002144Fascaplysin sensitizes cells to TRAIL-induced apoptosis through upregulating DR5 expression
Auteurs : Feng Wang [République populaire de Chine] ; Haimin Chen [République populaire de Chine] ; Xiaojun Yan [République populaire de Chine] ; Yanling Zheng [République populaire de Chine]Source :
- Chinese Journal of Oceanology and Limnology [ 0254-4059 ] ; 2013-05-01.
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Abstract
Abstract: This study investigated the molecular mechanism of anti-tumor effect of fascaplysin, a nitrogenous red pigment firstly isolated from a marine sponge. Microarray analysis show that the TNF and TNF receptor superfamily in human umbilical vein endothelial cells (HUVEC) and human hepatocarcinoma cells (BEL-7402) were significantly regulated by fascaplysin. Western Blot results reveal that fascaplysin increased the expression of cleaved caspase-9, active caspase-3, and decreased the level of procaspase-8 and Bid. Flow cytometry and cytotoxicity tests indicate that fascaplysin sensitized cells to tumor necrosis-related apoptosisinducing ligand-(TRAIL) induced apoptosis, which was markedly blocked by TRAIL R2/Fc chimera, a dominant negative form of TRAIL receptor DR5. Therefore, our results demonstrate that fascaplysin promotes apoptosis through the activation of TRAIL signaling pathway by upregulating DR5 expression.
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DOI: 10.1007/s00343-013-2215-y
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J. Ocean. Limnol.</title><idno type="ISSN">0254-4059</idno><idno type="eISSN">1993-5005</idno><imprint><publisher>SP Science Press</publisher><pubPlace>Heidelberg</pubPlace><date type="published" when="2013-05-01">2013-05-01</date><biblScope unit="volume">31</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="560">560</biblScope><biblScope unit="page" to="569">569</biblScope></imprint><idno type="ISSN">0254-4059</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0254-4059</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>DR5</term><term>TRAIL</term><term>apoptosis</term><term>fascaplysin</term><term>microarray</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: This study investigated the molecular mechanism of anti-tumor effect of fascaplysin, a nitrogenous red pigment firstly isolated from a marine sponge. Microarray analysis show that the TNF and TNF receptor superfamily in human umbilical vein endothelial cells (HUVEC) and human hepatocarcinoma cells (BEL-7402) were significantly regulated by fascaplysin. Western Blot results reveal that fascaplysin increased the expression of cleaved caspase-9, active caspase-3, and decreased the level of procaspase-8 and Bid. Flow cytometry and cytotoxicity tests indicate that fascaplysin sensitized cells to tumor necrosis-related apoptosisinducing ligand-(TRAIL) induced apoptosis, which was markedly blocked by TRAIL R2/Fc chimera, a dominant negative form of TRAIL receptor DR5. Therefore, our results demonstrate that fascaplysin promotes apoptosis through the activation of TRAIL signaling pathway by upregulating DR5 expression.</div></front></TEI><affiliations><list><country><li>République populaire de Chine</li></country></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Wang, Feng" sort="Wang, Feng" uniqKey="Wang F" first="Feng" last="Wang">Feng Wang</name></noRegion><name sortKey="Chen, Haimin" sort="Chen, Haimin" uniqKey="Chen H" first="Haimin" last="Chen">Haimin Chen</name><name sortKey="Chen, Haimin" sort="Chen, Haimin" uniqKey="Chen H" first="Haimin" last="Chen">Haimin Chen</name><name sortKey="Yan, Xiaojun" sort="Yan, Xiaojun" uniqKey="Yan X" first="Xiaojun" last="Yan">Xiaojun Yan</name><name sortKey="Zheng, Yanling" sort="Zheng, Yanling" uniqKey="Zheng Y" first="Yanling" last="Zheng">Yanling Zheng</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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