Mechanisms mediating the effects of IL-3 gene expression on tumor growth
IL‐3 gene expression within tumors leads to host‐cell infiltration, particularly by macrophages, slower tumor growth, and enhanced immunogenicity. Surprisingly, tumor‐associated macrophages (TAMs) from within FSAN‐JmIL3 tumors had decreased expression of TNF‐α and iNOS. On short‐term culture, TAMs f...
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| Veröffentlicht in: | Journal of leukocyte biology 2000-12, Vol.68 (6), p.890-896 |
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| container_title | Journal of leukocyte biology |
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| creator | Wu, Yuan‐Zhau Hong, Ji‐Hong Huang, Hsin‐Hong Dougherty, Graeme J. McBride, William H. Chiang, Chi‐Shiun |
| description | IL‐3 gene expression within tumors leads to host‐cell infiltration, particularly by macrophages, slower tumor growth, and enhanced immunogenicity. Surprisingly, tumor‐associated macrophages (TAMs) from within FSAN‐JmIL3 tumors had decreased expression of TNF‐α and iNOS. On short‐term culture, TAMs from FSAN‐JmIL3 tumors regained their capacity to produce TNF‐α and NO, indicating that they were primedin vivo. In vitro experiments were unable to demonstrate differences between FSAN‐JmIL3 and FSAN tumor cells in their ability to stimulate TNF‐α production by TAMs. In the absence of evidence that TAM activation was responsible for the slower growth of FSAN‐JmIL3 tumors, the response of tumor cells to these effector molecules was studied. TNF‐α and NO were cytotoxic for FSAN‐JmIL3 cells but growth stimulatory for FSAN. These tumor‐related phenotypic changes may contribute as much if not more than functional changes in host infiltrating cells to the slower growth of FSAN‐JmIL3 tumorsin vivo. |
| doi_str_mv | 10.1189/jlb.68.6.890 |
| format | Article |
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Surprisingly, tumor‐associated macrophages (TAMs) from within FSAN‐JmIL3 tumors had decreased expression of TNF‐α and iNOS. On short‐term culture, TAMs from FSAN‐JmIL3 tumors regained their capacity to produce TNF‐α and NO, indicating that they were primedin vivo. In vitro experiments were unable to demonstrate differences between FSAN‐JmIL3 and FSAN tumor cells in their ability to stimulate TNF‐α production by TAMs. In the absence of evidence that TAM activation was responsible for the slower growth of FSAN‐JmIL3 tumors, the response of tumor cells to these effector molecules was studied. TNF‐α and NO were cytotoxic for FSAN‐JmIL3 cells but growth stimulatory for FSAN. These tumor‐related phenotypic changes may contribute as much if not more than functional changes in host infiltrating cells to the slower growth of FSAN‐JmIL3 tumorsin vivo.</description><identifier>ISSN: 0741-5400</identifier><identifier>EISSN: 1938-3673</identifier><identifier>DOI: 10.1189/jlb.68.6.890</identifier><identifier>PMID: 11129657</identifier><language>eng</language><publisher>United States: Society for Leukocyte Biology</publisher><subject>Animals ; Apoptosis ; Cell Count ; cytokine ; Cytotoxicity, Immunologic ; Disease Progression ; DNA, Complementary - genetics ; Female ; Fibrosarcoma - chemically induced ; Fibrosarcoma - metabolism ; Fibrosarcoma - pathology ; Fibrosarcoma - secondary ; Gene Expression Regulation, Neoplastic ; immunotherapy ; iNOS ; Interleukin-3 - biosynthesis ; Interleukin-3 - genetics ; Interleukin-3 - physiology ; Lung Neoplasms - secondary ; Macrophages - physiology ; Mice ; Mice, Inbred C3H ; Neoplasm Proteins - biosynthesis ; Neoplasm Proteins - genetics ; Neoplasm Proteins - physiology ; Neoplasm Transplantation ; Nitric Oxide - biosynthesis ; Nitric Oxide - pharmacology ; Nitric Oxide Synthase - biosynthesis ; Nitric Oxide Synthase - genetics ; Nitric Oxide Synthase Type II ; Phenotype ; Recombinant Fusion Proteins - biosynthesis ; Recombinant Fusion Proteins - physiology ; RNA, Messenger - biosynthesis ; RNA, Neoplasm - biosynthesis ; TNF ; Transfection ; Tumor Cells, Cultured ; Tumor Necrosis Factor-alpha - biosynthesis ; Tumor Necrosis Factor-alpha - genetics ; Tumor Necrosis Factor-alpha - pharmacology</subject><ispartof>Journal of leukocyte biology, 2000-12, Vol.68 (6), p.890-896</ispartof><rights>2000 Society for Leukocyte Biology</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3900-244011c9d4f5e839228311277d00704475d50e54ee96171928776892e9523a4a3</citedby><cites>FETCH-LOGICAL-c3900-244011c9d4f5e839228311277d00704475d50e54ee96171928776892e9523a4a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1189%2Fjlb.68.6.890$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1189%2Fjlb.68.6.890$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>315,781,785,1418,27926,27927,45576,45577</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11129657$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wu, Yuan‐Zhau</creatorcontrib><creatorcontrib>Hong, Ji‐Hong</creatorcontrib><creatorcontrib>Huang, Hsin‐Hong</creatorcontrib><creatorcontrib>Dougherty, Graeme J.</creatorcontrib><creatorcontrib>McBride, William H.</creatorcontrib><creatorcontrib>Chiang, Chi‐Shiun</creatorcontrib><title>Mechanisms mediating the effects of IL-3 gene expression on tumor growth</title><title>Journal of leukocyte biology</title><addtitle>J Leukoc Biol</addtitle><description>IL‐3 gene expression within tumors leads to host‐cell infiltration, particularly by macrophages, slower tumor growth, and enhanced immunogenicity. Surprisingly, tumor‐associated macrophages (TAMs) from within FSAN‐JmIL3 tumors had decreased expression of TNF‐α and iNOS. On short‐term culture, TAMs from FSAN‐JmIL3 tumors regained their capacity to produce TNF‐α and NO, indicating that they were primedin vivo. In vitro experiments were unable to demonstrate differences between FSAN‐JmIL3 and FSAN tumor cells in their ability to stimulate TNF‐α production by TAMs. In the absence of evidence that TAM activation was responsible for the slower growth of FSAN‐JmIL3 tumors, the response of tumor cells to these effector molecules was studied. TNF‐α and NO were cytotoxic for FSAN‐JmIL3 cells but growth stimulatory for FSAN. These tumor‐related phenotypic changes may contribute as much if not more than functional changes in host infiltrating cells to the slower growth of FSAN‐JmIL3 tumorsin vivo.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Cell Count</subject><subject>cytokine</subject><subject>Cytotoxicity, Immunologic</subject><subject>Disease Progression</subject><subject>DNA, Complementary - genetics</subject><subject>Female</subject><subject>Fibrosarcoma - chemically induced</subject><subject>Fibrosarcoma - metabolism</subject><subject>Fibrosarcoma - pathology</subject><subject>Fibrosarcoma - secondary</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>immunotherapy</subject><subject>iNOS</subject><subject>Interleukin-3 - biosynthesis</subject><subject>Interleukin-3 - genetics</subject><subject>Interleukin-3 - physiology</subject><subject>Lung Neoplasms - secondary</subject><subject>Macrophages - physiology</subject><subject>Mice</subject><subject>Mice, Inbred C3H</subject><subject>Neoplasm Proteins - biosynthesis</subject><subject>Neoplasm Proteins - genetics</subject><subject>Neoplasm Proteins - physiology</subject><subject>Neoplasm Transplantation</subject><subject>Nitric Oxide - biosynthesis</subject><subject>Nitric Oxide - pharmacology</subject><subject>Nitric Oxide Synthase - biosynthesis</subject><subject>Nitric Oxide Synthase - genetics</subject><subject>Nitric Oxide Synthase Type II</subject><subject>Phenotype</subject><subject>Recombinant Fusion Proteins - biosynthesis</subject><subject>Recombinant Fusion Proteins - physiology</subject><subject>RNA, Messenger - biosynthesis</subject><subject>RNA, Neoplasm - biosynthesis</subject><subject>TNF</subject><subject>Transfection</subject><subject>Tumor Cells, Cultured</subject><subject>Tumor Necrosis Factor-alpha - biosynthesis</subject><subject>Tumor Necrosis Factor-alpha - genetics</subject><subject>Tumor Necrosis Factor-alpha - pharmacology</subject><issn>0741-5400</issn><issn>1938-3673</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kMtLw0AQhxdRtD5uniUXPZk6-8g-jipqlYoXPS8xnTRb8qi7KdH_3pUUvQkDA8M3vxk-Qk4pTCnV5mpVv0-lnsqpNrBDJtRwnXKp-C6ZgBI0zQTAATkMYQUAnEnYJweUUmZkpiZk9oxFlbcuNCFpcOHy3rXLpK8wwbLEog9JVyaP85QnS2zj8HPtMQTXtUmsftN0Pln6buirY7JX5nXAk20_Im_3d6-3s3T-8vB4ez1PC24AUiYEUFqYhSgz1Nwwpnl8RqkFgAIhVLbIADOBaCRV1DCtlNSGockYz0XOj8jFmLv23ccGQ28bFwqs67zFbhMsVSqjWvMIXo5g4bsQPJZ27V2T-y9Lwf6Ys9GcldpKG81F_Gybu3mPIv7graoI0BEYXI1f_4bZp_kNjKHn407lltXgPNrQ5HUdTzA7DMPv8W-KaYNH</recordid><startdate>200012</startdate><enddate>200012</enddate><creator>Wu, Yuan‐Zhau</creator><creator>Hong, Ji‐Hong</creator><creator>Huang, Hsin‐Hong</creator><creator>Dougherty, Graeme J.</creator><creator>McBride, William H.</creator><creator>Chiang, Chi‐Shiun</creator><general>Society for Leukocyte Biology</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>7T5</scope><scope>H94</scope></search><sort><creationdate>200012</creationdate><title>Mechanisms mediating the effects of IL-3 gene expression on tumor growth</title><author>Wu, Yuan‐Zhau ; Hong, Ji‐Hong ; Huang, Hsin‐Hong ; Dougherty, Graeme J. ; McBride, William H. ; Chiang, Chi‐Shiun</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3900-244011c9d4f5e839228311277d00704475d50e54ee96171928776892e9523a4a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>Animals</topic><topic>Apoptosis</topic><topic>Cell Count</topic><topic>cytokine</topic><topic>Cytotoxicity, Immunologic</topic><topic>Disease Progression</topic><topic>DNA, Complementary - genetics</topic><topic>Female</topic><topic>Fibrosarcoma - chemically induced</topic><topic>Fibrosarcoma - metabolism</topic><topic>Fibrosarcoma - pathology</topic><topic>Fibrosarcoma - secondary</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>immunotherapy</topic><topic>iNOS</topic><topic>Interleukin-3 - biosynthesis</topic><topic>Interleukin-3 - genetics</topic><topic>Interleukin-3 - physiology</topic><topic>Lung Neoplasms - secondary</topic><topic>Macrophages - physiology</topic><topic>Mice</topic><topic>Mice, Inbred C3H</topic><topic>Neoplasm Proteins - biosynthesis</topic><topic>Neoplasm Proteins - genetics</topic><topic>Neoplasm Proteins - physiology</topic><topic>Neoplasm Transplantation</topic><topic>Nitric Oxide - biosynthesis</topic><topic>Nitric Oxide - pharmacology</topic><topic>Nitric Oxide Synthase - biosynthesis</topic><topic>Nitric Oxide Synthase - genetics</topic><topic>Nitric Oxide Synthase Type II</topic><topic>Phenotype</topic><topic>Recombinant Fusion Proteins - biosynthesis</topic><topic>Recombinant Fusion Proteins - physiology</topic><topic>RNA, Messenger - biosynthesis</topic><topic>RNA, Neoplasm - biosynthesis</topic><topic>TNF</topic><topic>Transfection</topic><topic>Tumor Cells, Cultured</topic><topic>Tumor Necrosis Factor-alpha - biosynthesis</topic><topic>Tumor Necrosis Factor-alpha - genetics</topic><topic>Tumor Necrosis Factor-alpha - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wu, Yuan‐Zhau</creatorcontrib><creatorcontrib>Hong, Ji‐Hong</creatorcontrib><creatorcontrib>Huang, Hsin‐Hong</creatorcontrib><creatorcontrib>Dougherty, Graeme J.</creatorcontrib><creatorcontrib>McBride, William H.</creatorcontrib><creatorcontrib>Chiang, Chi‐Shiun</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><jtitle>Journal of leukocyte biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wu, Yuan‐Zhau</au><au>Hong, Ji‐Hong</au><au>Huang, Hsin‐Hong</au><au>Dougherty, Graeme J.</au><au>McBride, William H.</au><au>Chiang, Chi‐Shiun</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Mechanisms mediating the effects of IL-3 gene expression on tumor growth</atitle><jtitle>Journal of leukocyte biology</jtitle><addtitle>J Leukoc Biol</addtitle><date>2000-12</date><risdate>2000</risdate><volume>68</volume><issue>6</issue><spage>890</spage><epage>896</epage><pages>890-896</pages><issn>0741-5400</issn><eissn>1938-3673</eissn><abstract>IL‐3 gene expression within tumors leads to host‐cell infiltration, particularly by macrophages, slower tumor growth, and enhanced immunogenicity. Surprisingly, tumor‐associated macrophages (TAMs) from within FSAN‐JmIL3 tumors had decreased expression of TNF‐α and iNOS. On short‐term culture, TAMs from FSAN‐JmIL3 tumors regained their capacity to produce TNF‐α and NO, indicating that they were primedin vivo. In vitro experiments were unable to demonstrate differences between FSAN‐JmIL3 and FSAN tumor cells in their ability to stimulate TNF‐α production by TAMs. In the absence of evidence that TAM activation was responsible for the slower growth of FSAN‐JmIL3 tumors, the response of tumor cells to these effector molecules was studied. TNF‐α and NO were cytotoxic for FSAN‐JmIL3 cells but growth stimulatory for FSAN. These tumor‐related phenotypic changes may contribute as much if not more than functional changes in host infiltrating cells to the slower growth of FSAN‐JmIL3 tumorsin vivo.</abstract><cop>United States</cop><pub>Society for Leukocyte Biology</pub><pmid>11129657</pmid><doi>10.1189/jlb.68.6.890</doi><tpages>7</tpages></addata></record> |
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| ispartof | Journal of leukocyte biology, 2000-12, Vol.68 (6), p.890-896 |
| issn | 0741-5400 1938-3673 |
| language | eng |
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| source | Wiley Online Library - AutoHoldings Journals; MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Oxford University Press Journals All Titles (1996-Current) |
| subjects | Animals Apoptosis Cell Count cytokine Cytotoxicity, Immunologic Disease Progression DNA, Complementary - genetics Female Fibrosarcoma - chemically induced Fibrosarcoma - metabolism Fibrosarcoma - pathology Fibrosarcoma - secondary Gene Expression Regulation, Neoplastic immunotherapy iNOS Interleukin-3 - biosynthesis Interleukin-3 - genetics Interleukin-3 - physiology Lung Neoplasms - secondary Macrophages - physiology Mice Mice, Inbred C3H Neoplasm Proteins - biosynthesis Neoplasm Proteins - genetics Neoplasm Proteins - physiology Neoplasm Transplantation Nitric Oxide - biosynthesis Nitric Oxide - pharmacology Nitric Oxide Synthase - biosynthesis Nitric Oxide Synthase - genetics Nitric Oxide Synthase Type II Phenotype Recombinant Fusion Proteins - biosynthesis Recombinant Fusion Proteins - physiology RNA, Messenger - biosynthesis RNA, Neoplasm - biosynthesis TNF Transfection Tumor Cells, Cultured Tumor Necrosis Factor-alpha - biosynthesis Tumor Necrosis Factor-alpha - genetics Tumor Necrosis Factor-alpha - pharmacology |
| title | Mechanisms mediating the effects of IL-3 gene expression on tumor growth |
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