Signalling pathway of tumor necrosis factor in normal and tumor cells
Identifieur interne : 003154 ( Main/Exploration ); précédent : 003153; suivant : 003155Signalling pathway of tumor necrosis factor in normal and tumor cells
Auteurs : Naoki Watanabe [Japon] ; Hiroshi Neda [Japon] ; Yoshiki Ohtusuka [Japon] ; Hisao Sone [Japon] ; Naofumi Yamauchi [Japon] ; Masahiro Maeda [Japon] ; Hiroshi Kuriyama [Japon] ; Yoshiro Niitsu [Japon]Source :
- Cancer Immunology, Immunotherapy [ 0340-7004 ] ; 1989-03-01.
English descriptors
- Teeft :
- Acute lymphoblastic leukemia, Antitumor effect, Assay, Binding assay, Biol chem, Biol response, Cell lines, Cell proliferation, Cell surface, Cluster plates, Culture media, Culture medium, Culture plates, Cytotoxic, Cytotoxic effect, Cytotoxic mechanism, Cytotoxicity, Endoplasmic reticulum, Escherichia coli, Golgi bodies, Human diploid cells, Human tumor necrosis factor, Hypotonic buffer, Incubation, Incubation time, Internalization, Intracellular, Intracellular distribution, Lung cells, Lymphocyte, Lysosome, Lysosome fraction, Metabolic inhibitors, Necrosis, Neda, Niitsu, Normal cells, Percoll, Percoll density gradient, Percoll density gradient centrifugation, Peripheral lymphocytes, Prelysosomal fraction, Present study, Previous study, Proc natl acad, Rabbit tumor necrosis factor, Radioactivity, Receptor, Receptor number, Receptor numbers, Recombinant, Relative cytotoxicity, Same manner, Separate experiments, Sone, Specific activity, Specific binding, Specific binding assay, Sufficient condition, Tumor cells, Tumor necrosis factor, Watanabe, Yamauchi.
Abstract
Summary: Several aspects of the activity and effects of tumor necrosis factor (TNF) were investigated to gain further insight into its cytotoxic mechanism. The relation between number of TNF receptors and TNF susceptibility of both tumor cells and normal cells was studied, utilizing a specific binding assay. Among the tumor cells, a fairly close correlation (r=0.855) was observed between receptor number and sensitivity to TNF. No cytotoxic effect by TNF was observed on any of the normal cells tested, even though TNF receptors were shown to be present, and cell proliferation was apparently stimulated by TNF in some cases. TNF internalization and intracellular distribution were studied by pulse-labelling and Percoll density gradient centrifugation. In L-M (murine tumorigenic fibroblasts, highly sensitive to TNF cytotoxicity) cells and HEL (human embryonic lung cells, non-sensitive to TNF cytotoxicity) cells, receptor-bound 125I-labelled recombinant human TNF was rapidly internalized and delivered to lysosomes within 15–30 min, and this was followed by degradation and release into the culture medium. The presence of either a cytoskeletal disrupting agent or a lysosomotropic agent was observed to inhibit the cytotoxic effect of TNF, thus also indicating that TNF internalization, followed by delivery to lysosomes, is essential in the cytolytic mechanism of TNF. As observed by [3H]uridine incorporation, TNF did not affect RNA synthesis in L-R cells (TNF-resistant cell lines derived from L-M cells) and HEL cells, but markedly stimulated (by 3.5 times) RNA synthesis in L-M cells.
Url:
DOI: 10.1007/BF00204983
Affiliations:
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first="Hiroshi" last="Kuriyama">Hiroshi Kuriyama</name><affiliation wicri:level="1"><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Internal Medicine (Section 4) Sapporo Medical College, South-1, West-16 Chuo-ku, 060, Sapporo</wicri:regionArea><wicri:noRegion>Sapporo</wicri:noRegion></affiliation></author><author><name sortKey="Niitsu, Yoshiro" sort="Niitsu, Yoshiro" uniqKey="Niitsu Y" first="Yoshiro" last="Niitsu">Yoshiro Niitsu</name><affiliation wicri:level="1"><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Internal Medicine (Section 4) Sapporo Medical College, South-1, West-16 Chuo-ku, 060, Sapporo</wicri:regionArea><wicri:noRegion>Sapporo</wicri:noRegion></affiliation></author></analytic><monogr></monogr><series><title level="j">Cancer Immunology, Immunotherapy</title><title level="j" type="abbrev">Cancer Immunol Immunother</title><idno type="ISSN">0340-7004</idno><idno type="eISSN">1432-0851</idno><imprint><publisher>Springer-Verlag</publisher><pubPlace>Berlin/Heidelberg</pubPlace><date type="published" when="1989-03-01">1989-03-01</date><biblScope unit="volume">28</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="157">157</biblScope><biblScope unit="page" to="163">163</biblScope></imprint><idno type="ISSN">0340-7004</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0340-7004</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Acute lymphoblastic leukemia</term><term>Antitumor effect</term><term>Assay</term><term>Binding assay</term><term>Biol chem</term><term>Biol response</term><term>Cell lines</term><term>Cell proliferation</term><term>Cell surface</term><term>Cluster plates</term><term>Culture media</term><term>Culture medium</term><term>Culture plates</term><term>Cytotoxic</term><term>Cytotoxic effect</term><term>Cytotoxic mechanism</term><term>Cytotoxicity</term><term>Endoplasmic reticulum</term><term>Escherichia coli</term><term>Golgi bodies</term><term>Human diploid cells</term><term>Human tumor necrosis factor</term><term>Hypotonic buffer</term><term>Incubation</term><term>Incubation time</term><term>Internalization</term><term>Intracellular</term><term>Intracellular distribution</term><term>Lung cells</term><term>Lymphocyte</term><term>Lysosome</term><term>Lysosome fraction</term><term>Metabolic inhibitors</term><term>Necrosis</term><term>Neda</term><term>Niitsu</term><term>Normal cells</term><term>Percoll</term><term>Percoll density gradient</term><term>Percoll density gradient centrifugation</term><term>Peripheral lymphocytes</term><term>Prelysosomal fraction</term><term>Present study</term><term>Previous study</term><term>Proc natl acad</term><term>Rabbit tumor necrosis factor</term><term>Radioactivity</term><term>Receptor</term><term>Receptor number</term><term>Receptor numbers</term><term>Recombinant</term><term>Relative cytotoxicity</term><term>Same manner</term><term>Separate experiments</term><term>Sone</term><term>Specific activity</term><term>Specific binding</term><term>Specific binding assay</term><term>Sufficient condition</term><term>Tumor cells</term><term>Tumor necrosis factor</term><term>Watanabe</term><term>Yamauchi</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Summary: Several aspects of the activity and effects of tumor necrosis factor (TNF) were investigated to gain further insight into its cytotoxic mechanism. The relation between number of TNF receptors and TNF susceptibility of both tumor cells and normal cells was studied, utilizing a specific binding assay. Among the tumor cells, a fairly close correlation (r=0.855) was observed between receptor number and sensitivity to TNF. No cytotoxic effect by TNF was observed on any of the normal cells tested, even though TNF receptors were shown to be present, and cell proliferation was apparently stimulated by TNF in some cases. TNF internalization and intracellular distribution were studied by pulse-labelling and Percoll density gradient centrifugation. In L-M (murine tumorigenic fibroblasts, highly sensitive to TNF cytotoxicity) cells and HEL (human embryonic lung cells, non-sensitive to TNF cytotoxicity) cells, receptor-bound 125I-labelled recombinant human TNF was rapidly internalized and delivered to lysosomes within 15–30 min, and this was followed by degradation and release into the culture medium. The presence of either a cytoskeletal disrupting agent or a lysosomotropic agent was observed to inhibit the cytotoxic effect of TNF, thus also indicating that TNF internalization, followed by delivery to lysosomes, is essential in the cytolytic mechanism of TNF. As observed by [3H]uridine incorporation, TNF did not affect RNA synthesis in L-R cells (TNF-resistant cell lines derived from L-M cells) and HEL cells, but markedly stimulated (by 3.5 times) RNA synthesis in L-M cells.</div></front></TEI><affiliations><list><country><li>Japon</li></country></list><tree><country name="Japon"><noRegion><name sortKey="Watanabe, Naoki" sort="Watanabe, Naoki" uniqKey="Watanabe N" first="Naoki" last="Watanabe">Naoki Watanabe</name></noRegion><name sortKey="Kuriyama, Hiroshi" sort="Kuriyama, Hiroshi" uniqKey="Kuriyama H" first="Hiroshi" last="Kuriyama">Hiroshi Kuriyama</name><name sortKey="Maeda, Masahiro" sort="Maeda, Masahiro" uniqKey="Maeda M" first="Masahiro" last="Maeda">Masahiro Maeda</name><name sortKey="Neda, Hiroshi" sort="Neda, Hiroshi" uniqKey="Neda H" first="Hiroshi" last="Neda">Hiroshi Neda</name><name sortKey="Niitsu, Yoshiro" sort="Niitsu, Yoshiro" uniqKey="Niitsu Y" first="Yoshiro" last="Niitsu">Yoshiro Niitsu</name><name sortKey="Ohtusuka, Yoshiki" sort="Ohtusuka, Yoshiki" uniqKey="Ohtusuka Y" first="Yoshiki" last="Ohtusuka">Yoshiki Ohtusuka</name><name sortKey="Sone, Hisao" sort="Sone, Hisao" uniqKey="Sone H" first="Hisao" last="Sone">Hisao Sone</name><name sortKey="Yamauchi, Naofumi" sort="Yamauchi, Naofumi" uniqKey="Yamauchi N" first="Naofumi" last="Yamauchi">Naofumi Yamauchi</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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