Mechanism of Fas‐mediated cell death and its enhancement by TNF‐α in human salivary gland adenocarcinoma cell line HSG
Identifieur interne : 000475 ( Main/Exploration ); précédent : 000474; suivant : 000476Mechanism of Fas‐mediated cell death and its enhancement by TNF‐α in human salivary gland adenocarcinoma cell line HSG
Auteurs : Naoyuki Chosa [Japon] ; Seiko Kyakumoto [Japon] ; Noriko Kito [Japon] ; Masaharu Kamo [Japon] ; Nobuko Sato [Japon]Source :
- European Journal of Oral Sciences [ 0909-8836 ] ; 2004-08.
English descriptors
Abstract
Fas‐mediated cell death in a human salivary gland adenocarcinoma cell line (HSG) was induced by treatment of the cells with agonistic anti‐Fas antibody (CH‐11), and this cell death was enhanced by pretreatment with tumor necrosis factor alpha (TNF‐α). The mode of cell death was apoptosis, because it was accompanied by caspase activation and the cleavage of poly(ADP‐ribose) polymerase. The TNF‐α treatment of the cells increased the expression of Fas, which was accompanied by the activation of nuclear factor κB (NFκB). These results suggest that the enhancement of the apoptosis caused by TNF‐α resulted from increased sensitivity of the HSG cells to CH‐11‐mediated apoptosis due to induction of Fas protein by TNF‐α via the activation of NFκB. In order to elucidate the apoptosis signaling pathway, we examined the effect of various caspase inhibitors on the apoptosis induced by CH‐11. Fas‐mediated apoptosis of HSG cells was slightly inhibited by the caspase‐9 inhibitor although it was mainly inhibited by that for caspase‐8. Based on this finding, we consider CH‐11‐induced apoptosis in HSG cells to be mainly mediated by the type I death signaling pathway that is caused by a caspase cascade initiated by the activation of caspase‐8 at the death‐inducing signaling complex (DISC).
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DOI: 10.1111/j.1600-0722.2004.00145.x
Affiliations:
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Chosa</name><affiliation wicri:level="1"><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Biochemistry, Iwate Medical University School of Dentistry, Morioka, Iwate</wicri:regionArea><wicri:noRegion>Iwate</wicri:noRegion></affiliation><affiliation><wicri:noCountry code="no comma">These authors contributed equally to this work.</wicri:noCountry></affiliation></author><author><name sortKey="Kyakumoto, Seiko" sort="Kyakumoto, Seiko" uniqKey="Kyakumoto S" first="Seiko" last="Kyakumoto">Seiko Kyakumoto</name><affiliation wicri:level="1"><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Biochemistry, Iwate Medical University School of Dentistry, Morioka, Iwate</wicri:regionArea><wicri:noRegion>Iwate</wicri:noRegion></affiliation><affiliation><wicri:noCountry code="no comma">These authors contributed equally to this work.</wicri:noCountry></affiliation></author><author><name sortKey="Kito, Noriko" sort="Kito, Noriko" uniqKey="Kito N" first="Noriko" last="Kito">Noriko Kito</name><affiliation wicri:level="1"><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Biochemistry, Iwate Medical University School of Dentistry, Morioka, Iwate</wicri:regionArea><wicri:noRegion>Iwate</wicri:noRegion></affiliation></author><author><name sortKey="Kamo, Masaharu" sort="Kamo, Masaharu" uniqKey="Kamo M" first="Masaharu" last="Kamo">Masaharu Kamo</name><affiliation wicri:level="1"><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Biochemistry, Iwate Medical University School of Dentistry, Morioka, Iwate</wicri:regionArea><wicri:noRegion>Iwate</wicri:noRegion></affiliation></author><author><name sortKey="Sato, Nobuko" sort="Sato, Nobuko" uniqKey="Sato N" first="Nobuko" last="Sato">Nobuko Sato</name><affiliation wicri:level="1"><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Biochemistry, Iwate Medical University School of Dentistry, Morioka, 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xml:lang="en"><term>Fas</term><term>HSG</term><term>caspase</term><term>nuclear factor κB (NFκB)</term><term>tumor necrosis factor alpha (TNF‐α)</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Fas‐mediated cell death in a human salivary gland adenocarcinoma cell line (HSG) was induced by treatment of the cells with agonistic anti‐Fas antibody (CH‐11), and this cell death was enhanced by pretreatment with tumor necrosis factor alpha (TNF‐α). The mode of cell death was apoptosis, because it was accompanied by caspase activation and the cleavage of poly(ADP‐ribose) polymerase. The TNF‐α treatment of the cells increased the expression of Fas, which was accompanied by the activation of nuclear factor κB (NFκB). These results suggest that the enhancement of the apoptosis caused by TNF‐α resulted from increased sensitivity of the HSG cells to CH‐11‐mediated apoptosis due to induction of Fas protein by TNF‐α via the activation of NFκB. In order to elucidate the apoptosis signaling pathway, we examined the effect of various caspase inhibitors on the apoptosis induced by CH‐11. Fas‐mediated apoptosis of HSG cells was slightly inhibited by the caspase‐9 inhibitor although it was mainly inhibited by that for caspase‐8. Based on this finding, we consider CH‐11‐induced apoptosis in HSG cells to be mainly mediated by the type I death signaling pathway that is caused by a caspase cascade initiated by the activation of caspase‐8 at the death‐inducing signaling complex (DISC).</div></front></TEI><affiliations><list><country><li>Japon</li></country></list><tree><country name="Japon"><noRegion><name sortKey="Chosa, Naoyuki" sort="Chosa, Naoyuki" uniqKey="Chosa N" first="Naoyuki" last="Chosa">Naoyuki Chosa</name></noRegion><name sortKey="Kamo, Masaharu" sort="Kamo, Masaharu" uniqKey="Kamo M" first="Masaharu" last="Kamo">Masaharu Kamo</name><name sortKey="Kito, Noriko" sort="Kito, Noriko" uniqKey="Kito N" first="Noriko" last="Kito">Noriko Kito</name><name sortKey="Kyakumoto, Seiko" sort="Kyakumoto, Seiko" uniqKey="Kyakumoto S" first="Seiko" last="Kyakumoto">Seiko Kyakumoto</name><name sortKey="Sato, Nobuko" sort="Sato, Nobuko" uniqKey="Sato N" first="Nobuko" last="Sato">Nobuko Sato</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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