Rat colon carcinoma cells that survived systemic immune surveillance are less sensitive to NK-cell mediated apoptosis
In order to form distant metastases, cells from the primary tumor have to detach, enter the blood- or lymph-compartment and escape immune surveillance. Here, we describe the selection of rat colon carcinoma cell lines (CC531s-m1 and CC531s-m2) that escaped from systemic immune surveillance; CC531s c...
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| Veröffentlicht in: | Clinical & experimental metastasis 2003-01, Vol.20 (8), p.713-722 |
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| creator | Velthuis, Jurjen H L Stitzinger, Miranda Aalbers, Remco I J M de Bont, Hans J G M Mulder, Gerard J Kuppen, Peter J K Nagelkerke, J Fred |
| description | In order to form distant metastases, cells from the primary tumor have to detach, enter the blood- or lymph-compartment and escape immune surveillance. Here, we describe the selection of rat colon carcinoma cell lines (CC531s-m1 and CC531s-m2) that escaped from systemic immune surveillance; CC531s cells were injected into the v. jugularis of Wag/Rij rats, after three weeks the lung tumors were isolated, the tumor cells were cultured, characterized and injected again. The m1- and m2-cell lines were less susceptible for killing by syngeneic NK cells. Further characterization of this cell line showed a decreased sensitivity towards TRAIL- and CD95L-, but not to granzyme B-mediated apoptosis. In the m1- and m2-cells log-phase growth started earlier as compared to the parental cell line, whereas no changes were found in anchorage-dependent or anchorage-independent growth. After subcapsular injection of the m2-cell line into the liver of rats much more lung metastases were formed in comparison to injection of the parental cell line. In conclusion, the results suggest that the resistance of the m1- and m2-cells to NK cell-mediated apoptosis was associated with their capability to survive systemic immune surveillance and form metastases in vivo. |
| doi_str_mv | 10.1023/B:CLIN.0000006818.27267.03 |
| format | Article |
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Here, we describe the selection of rat colon carcinoma cell lines (CC531s-m1 and CC531s-m2) that escaped from systemic immune surveillance; CC531s cells were injected into the v. jugularis of Wag/Rij rats, after three weeks the lung tumors were isolated, the tumor cells were cultured, characterized and injected again. The m1- and m2-cell lines were less susceptible for killing by syngeneic NK cells. Further characterization of this cell line showed a decreased sensitivity towards TRAIL- and CD95L-, but not to granzyme B-mediated apoptosis. In the m1- and m2-cells log-phase growth started earlier as compared to the parental cell line, whereas no changes were found in anchorage-dependent or anchorage-independent growth. After subcapsular injection of the m2-cell line into the liver of rats much more lung metastases were formed in comparison to injection of the parental cell line. In conclusion, the results suggest that the resistance of the m1- and m2-cells to NK cell-mediated apoptosis was associated with their capability to survive systemic immune surveillance and form metastases in vivo.</description><identifier>ISSN: 0262-0898</identifier><identifier>EISSN: 1573-7276</identifier><identifier>DOI: 10.1023/B:CLIN.0000006818.27267.03</identifier><identifier>PMID: 14713105</identifier><identifier>CODEN: CEXMD2</identifier><language>eng</language><publisher>Netherlands: Springer Nature B.V</publisher><subject>Animals ; Apoptosis ; Cell Adhesion ; Colonic Neoplasms - immunology ; Cytotoxicity, Immunologic ; Killer Cells, Natural - immunology ; Lung Neoplasms - secondary ; Male ; Rats ; Tumor Cells, Cultured</subject><ispartof>Clinical & experimental metastasis, 2003-01, Vol.20 (8), p.713-722</ispartof><rights>Copyright Kluwer Academic Publishers 2003</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c373t-a9bbb793166ec5428660b5fc5f1ffb2d37b0070a526823e7d352c834b3c1ab193</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/14713105$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Velthuis, Jurjen H L</creatorcontrib><creatorcontrib>Stitzinger, Miranda</creatorcontrib><creatorcontrib>Aalbers, Remco I J M</creatorcontrib><creatorcontrib>de Bont, Hans J G M</creatorcontrib><creatorcontrib>Mulder, Gerard J</creatorcontrib><creatorcontrib>Kuppen, Peter J K</creatorcontrib><creatorcontrib>Nagelkerke, J Fred</creatorcontrib><title>Rat colon carcinoma cells that survived systemic immune surveillance are less sensitive to NK-cell mediated apoptosis</title><title>Clinical & experimental metastasis</title><addtitle>Clin Exp Metastasis</addtitle><description>In order to form distant metastases, cells from the primary tumor have to detach, enter the blood- or lymph-compartment and escape immune surveillance. Here, we describe the selection of rat colon carcinoma cell lines (CC531s-m1 and CC531s-m2) that escaped from systemic immune surveillance; CC531s cells were injected into the v. jugularis of Wag/Rij rats, after three weeks the lung tumors were isolated, the tumor cells were cultured, characterized and injected again. The m1- and m2-cell lines were less susceptible for killing by syngeneic NK cells. Further characterization of this cell line showed a decreased sensitivity towards TRAIL- and CD95L-, but not to granzyme B-mediated apoptosis. In the m1- and m2-cells log-phase growth started earlier as compared to the parental cell line, whereas no changes were found in anchorage-dependent or anchorage-independent growth. After subcapsular injection of the m2-cell line into the liver of rats much more lung metastases were formed in comparison to injection of the parental cell line. In conclusion, the results suggest that the resistance of the m1- and m2-cells to NK cell-mediated apoptosis was associated with their capability to survive systemic immune surveillance and form metastases in vivo.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Cell Adhesion</subject><subject>Colonic Neoplasms - immunology</subject><subject>Cytotoxicity, Immunologic</subject><subject>Killer Cells, Natural - immunology</subject><subject>Lung Neoplasms - secondary</subject><subject>Male</subject><subject>Rats</subject><subject>Tumor Cells, Cultured</subject><issn>0262-0898</issn><issn>1573-7276</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqFkU1PGzEQhq2KqgTav1BZHLht8Mf6Y7lB1AIiolLVni3b8apGu-vU40Xi3-OESEhcmIsP87zvjOdF6IySJSWMX1xfrtZ3D0uyL6mpXjLFpFoS_gktqFC8UUzJI7QgTLKG6E4foxOAx0q3Sukv6Ji2inJKxALNv23BPg1pwt5mH6c0WuzDMAAu_2oL5vwUn8IGwzOUMEaP4zjOU9g3QhwGO_mAbQ54CAAYwgSxVAEuCT_cNzsnPIZNtKV62G3algQRvqLPvR0gfDu8p-jvzx9_VrfN-tfN3epq3XiueGls55xTHadSBi9apqUkTvRe9LTvHdtw5QhRxAomNeNBbbhgXvPWcU-tox0_Reevvtuc_s8Bihkj7HayU0gzGEUF4Z3UH4K0U5xIIit49g58THOe6icMoy0VXT19hS5fIZ8TQA692eY42vxsKDG7CM212UVo3iI0-wgN4VX8_TBhdvVyb9JDZvwFR9WY5Q</recordid><startdate>20030101</startdate><enddate>20030101</enddate><creator>Velthuis, Jurjen H L</creator><creator>Stitzinger, Miranda</creator><creator>Aalbers, Remco I J M</creator><creator>de Bont, Hans J G M</creator><creator>Mulder, Gerard J</creator><creator>Kuppen, Peter J K</creator><creator>Nagelkerke, J Fred</creator><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7TO</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8FE</scope><scope>8FG</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>P5Z</scope><scope>P62</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7T5</scope><scope>7X8</scope></search><sort><creationdate>20030101</creationdate><title>Rat colon carcinoma cells that survived systemic immune surveillance are less sensitive to NK-cell mediated apoptosis</title><author>Velthuis, Jurjen H L ; 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In conclusion, the results suggest that the resistance of the m1- and m2-cells to NK cell-mediated apoptosis was associated with their capability to survive systemic immune surveillance and form metastases in vivo.</abstract><cop>Netherlands</cop><pub>Springer Nature B.V</pub><pmid>14713105</pmid><doi>10.1023/B:CLIN.0000006818.27267.03</doi><tpages>10</tpages></addata></record> |
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| ispartof | Clinical & experimental metastasis, 2003-01, Vol.20 (8), p.713-722 |
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| source | MEDLINE; SpringerNature Journals |
| subjects | Animals Apoptosis Cell Adhesion Colonic Neoplasms - immunology Cytotoxicity, Immunologic Killer Cells, Natural - immunology Lung Neoplasms - secondary Male Rats Tumor Cells, Cultured |
| title | Rat colon carcinoma cells that survived systemic immune surveillance are less sensitive to NK-cell mediated apoptosis |
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