Induction of Vascular Endothelial Growth Factor by Insulin-like Growth Factor 1 in Colorectal Carcinoma
Vascular endothelial growth factor (VEGF) is an angiogenic hormone that is produced by and supports the growth of many types of malignancies. The present study shows that insulin-like growth factor 1 (IGF-I), a mitogen that promotes the propagation of cancers through autocrine and paracrine mechanis...
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| Veröffentlicht in: | The Journal of biological chemistry 1996-11, Vol.271 (46), p.29483-29488 |
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| creator | Warren, R S Yuan, H Matli, M R Ferrara, N Donner, D B |
| description | Vascular endothelial growth factor (VEGF) is an angiogenic hormone that is produced by and supports the growth of many types
of malignancies. The present study shows that insulin-like growth factor 1 (IGF-I), a mitogen that promotes the propagation
of cancers through autocrine and paracrine mechanisms, increases the expression of mRNA for VEGF and production of VEGF protein
by COLO 205 colon carcinoma cells. IGF-I also induces expression of VEGF mRNA in SW620, LSLiM6, and HCT15 colon carcinoma
cells showing that this is a common response to IGF-I. Whereas IGF-I induced VEGF mRNA in each cell line examined (2.3-12-fold),
it induced proliferation only in COLO 205 and LSLiM6 cells. Thus, the proliferative response induced by IGF-I and its ability
to induce VEGF occur through distinguishable mechanisms. IGF-I increases the cellular content of VEGF mRNA by increasing the
rate of transcription (5-fold after 4 h) and also by increasing the half-life of VEGF mRNA (0.6 ± 0.07 h in control cells
to 2.0 ± 0.37 h in IGF-I-treated cells). Monoclonal antibody (αIR3) directed against the type 1 IGF receptor significantly
attenuated the ability of IGF-I to promote expression of VEGF mRNA. Interestingly, by itself αIR3 acted as a weak agonist
and induced a modest increase in the cellular content of VEGF mRNA. αIR3 also promoted tyrosine phosphorylation of the β subunit
of the IGF-I receptor, and the magnitude of this response was comparable with that induced by IGF-I. These observations point
to a nonlinear relationship between activation of the IGF-I receptor and induction of VEGF mRNA. Thus, in addition to its
direct, growth stimulatory effect on transformed cells, IGF-I induces the expression of VEGF which can promote the progression
of cancer by regulating the development of new blood vessels. |
| doi_str_mv | 10.1074/jbc.271.46.29483 |
| format | Article |
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of malignancies. The present study shows that insulin-like growth factor 1 (IGF-I), a mitogen that promotes the propagation
of cancers through autocrine and paracrine mechanisms, increases the expression of mRNA for VEGF and production of VEGF protein
by COLO 205 colon carcinoma cells. IGF-I also induces expression of VEGF mRNA in SW620, LSLiM6, and HCT15 colon carcinoma
cells showing that this is a common response to IGF-I. Whereas IGF-I induced VEGF mRNA in each cell line examined (2.3-12-fold),
it induced proliferation only in COLO 205 and LSLiM6 cells. Thus, the proliferative response induced by IGF-I and its ability
to induce VEGF occur through distinguishable mechanisms. IGF-I increases the cellular content of VEGF mRNA by increasing the
rate of transcription (5-fold after 4 h) and also by increasing the half-life of VEGF mRNA (0.6 ± 0.07 h in control cells
to 2.0 ± 0.37 h in IGF-I-treated cells). Monoclonal antibody (αIR3) directed against the type 1 IGF receptor significantly
attenuated the ability of IGF-I to promote expression of VEGF mRNA. Interestingly, by itself αIR3 acted as a weak agonist
and induced a modest increase in the cellular content of VEGF mRNA. αIR3 also promoted tyrosine phosphorylation of the β subunit
of the IGF-I receptor, and the magnitude of this response was comparable with that induced by IGF-I. These observations point
to a nonlinear relationship between activation of the IGF-I receptor and induction of VEGF mRNA. Thus, in addition to its
direct, growth stimulatory effect on transformed cells, IGF-I induces the expression of VEGF which can promote the progression
of cancer by regulating the development of new blood vessels.</description><identifier>ISSN: 0021-9258</identifier><identifier>EISSN: 1083-351X</identifier><identifier>DOI: 10.1074/jbc.271.46.29483</identifier><identifier>PMID: 8910616</identifier><language>eng</language><publisher>United States: American Society for Biochemistry and Molecular Biology</publisher><subject>Colorectal Neoplasms - metabolism ; Colorectal Neoplasms - pathology ; Endothelial Growth Factors - biosynthesis ; Endothelial Growth Factors - genetics ; Gene Expression Regulation - physiology ; Humans ; Insulin-Like Growth Factor I - physiology ; Lymphokines - biosynthesis ; Lymphokines - genetics ; RNA, Messenger - genetics ; RNA, Messenger - metabolism ; Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factors</subject><ispartof>The Journal of biological chemistry, 1996-11, Vol.271 (46), p.29483-29488</ispartof><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c462t-300f036fe2c8d0b062bad33690eca1fc75a72f986c8b6a0af9d9c64e13babcf23</citedby><cites>FETCH-LOGICAL-c462t-300f036fe2c8d0b062bad33690eca1fc75a72f986c8b6a0af9d9c64e13babcf23</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27903,27904</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8910616$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Warren, R S</creatorcontrib><creatorcontrib>Yuan, H</creatorcontrib><creatorcontrib>Matli, M R</creatorcontrib><creatorcontrib>Ferrara, N</creatorcontrib><creatorcontrib>Donner, D B</creatorcontrib><title>Induction of Vascular Endothelial Growth Factor by Insulin-like Growth Factor 1 in Colorectal Carcinoma</title><title>The Journal of biological chemistry</title><addtitle>J Biol Chem</addtitle><description>Vascular endothelial growth factor (VEGF) is an angiogenic hormone that is produced by and supports the growth of many types
of malignancies. The present study shows that insulin-like growth factor 1 (IGF-I), a mitogen that promotes the propagation
of cancers through autocrine and paracrine mechanisms, increases the expression of mRNA for VEGF and production of VEGF protein
by COLO 205 colon carcinoma cells. IGF-I also induces expression of VEGF mRNA in SW620, LSLiM6, and HCT15 colon carcinoma
cells showing that this is a common response to IGF-I. Whereas IGF-I induced VEGF mRNA in each cell line examined (2.3-12-fold),
it induced proliferation only in COLO 205 and LSLiM6 cells. Thus, the proliferative response induced by IGF-I and its ability
to induce VEGF occur through distinguishable mechanisms. IGF-I increases the cellular content of VEGF mRNA by increasing the
rate of transcription (5-fold after 4 h) and also by increasing the half-life of VEGF mRNA (0.6 ± 0.07 h in control cells
to 2.0 ± 0.37 h in IGF-I-treated cells). Monoclonal antibody (αIR3) directed against the type 1 IGF receptor significantly
attenuated the ability of IGF-I to promote expression of VEGF mRNA. Interestingly, by itself αIR3 acted as a weak agonist
and induced a modest increase in the cellular content of VEGF mRNA. αIR3 also promoted tyrosine phosphorylation of the β subunit
of the IGF-I receptor, and the magnitude of this response was comparable with that induced by IGF-I. These observations point
to a nonlinear relationship between activation of the IGF-I receptor and induction of VEGF mRNA. Thus, in addition to its
direct, growth stimulatory effect on transformed cells, IGF-I induces the expression of VEGF which can promote the progression
of cancer by regulating the development of new blood vessels.</description><subject>Colorectal Neoplasms - metabolism</subject><subject>Colorectal Neoplasms - pathology</subject><subject>Endothelial Growth Factors - biosynthesis</subject><subject>Endothelial Growth Factors - genetics</subject><subject>Gene Expression Regulation - physiology</subject><subject>Humans</subject><subject>Insulin-Like Growth Factor I - physiology</subject><subject>Lymphokines - biosynthesis</subject><subject>Lymphokines - genetics</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Messenger - metabolism</subject><subject>Vascular Endothelial Growth Factor A</subject><subject>Vascular Endothelial Growth Factors</subject><issn>0021-9258</issn><issn>1083-351X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1996</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkb1r3DAYxkVoSC8fe5aChtLNjl7JluWxHPk4OOiShGxCkqVYqWxdJZuQ_75O7ii0S9_lGZ6P4f0hdAmkBNJUVy_alLSBsuIlbSvBjtAKiGAFq-HpE1oRQqFoaS0-o9OcX8hyVQsn6ES0QDjwFXrejN1sJh9HHB1-VNnMQSV8PXZx6m3wKuDbFF-nHt8oM8WE9RvejHkOfiyC_2n_cQH7Ea9jiMmaaemuVTJ-jIM6R8dOhWwvDnqGHm6u79d3xfbH7Wb9fVuYitOpYIQ4wriz1IiOaMKpVh1jvCXWKHCmqVVDXSu4EZorolzbtYZXFphW2jjKztC3_e4uxV-zzZMcfDY2BDXaOGfZiJqCAPHfINRNw5mAJUj2QZNizsk6uUt-UOlNApHvEOQCQS4QZMXlB4Sl8uWwPevBdn8Kh68v_te93_vn_tUnK7WPprfD3zO_AcAzj4s</recordid><startdate>19961115</startdate><enddate>19961115</enddate><creator>Warren, R S</creator><creator>Yuan, H</creator><creator>Matli, M R</creator><creator>Ferrara, N</creator><creator>Donner, D B</creator><general>American Society for Biochemistry and Molecular 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>7TO</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>19961115</creationdate><title>Induction of Vascular Endothelial Growth Factor by Insulin-like Growth Factor 1 in Colorectal Carcinoma</title><author>Warren, R S ; Yuan, H ; Matli, M R ; Ferrara, N ; Donner, D B</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c462t-300f036fe2c8d0b062bad33690eca1fc75a72f986c8b6a0af9d9c64e13babcf23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1996</creationdate><topic>Colorectal Neoplasms - metabolism</topic><topic>Colorectal Neoplasms - pathology</topic><topic>Endothelial Growth Factors - biosynthesis</topic><topic>Endothelial Growth Factors - genetics</topic><topic>Gene Expression Regulation - physiology</topic><topic>Humans</topic><topic>Insulin-Like Growth Factor I - physiology</topic><topic>Lymphokines - biosynthesis</topic><topic>Lymphokines - genetics</topic><topic>RNA, Messenger - genetics</topic><topic>RNA, Messenger - metabolism</topic><topic>Vascular Endothelial Growth Factor A</topic><topic>Vascular Endothelial Growth Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Warren, R S</creatorcontrib><creatorcontrib>Yuan, H</creatorcontrib><creatorcontrib>Matli, M R</creatorcontrib><creatorcontrib>Ferrara, N</creatorcontrib><creatorcontrib>Donner, D B</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>The Journal of biological chemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Warren, R S</au><au>Yuan, H</au><au>Matli, M R</au><au>Ferrara, N</au><au>Donner, D B</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Induction of Vascular Endothelial Growth Factor by Insulin-like Growth Factor 1 in Colorectal Carcinoma</atitle><jtitle>The Journal of biological chemistry</jtitle><addtitle>J Biol Chem</addtitle><date>1996-11-15</date><risdate>1996</risdate><volume>271</volume><issue>46</issue><spage>29483</spage><epage>29488</epage><pages>29483-29488</pages><issn>0021-9258</issn><eissn>1083-351X</eissn><abstract>Vascular endothelial growth factor (VEGF) is an angiogenic hormone that is produced by and supports the growth of many types
of malignancies. The present study shows that insulin-like growth factor 1 (IGF-I), a mitogen that promotes the propagation
of cancers through autocrine and paracrine mechanisms, increases the expression of mRNA for VEGF and production of VEGF protein
by COLO 205 colon carcinoma cells. IGF-I also induces expression of VEGF mRNA in SW620, LSLiM6, and HCT15 colon carcinoma
cells showing that this is a common response to IGF-I. Whereas IGF-I induced VEGF mRNA in each cell line examined (2.3-12-fold),
it induced proliferation only in COLO 205 and LSLiM6 cells. Thus, the proliferative response induced by IGF-I and its ability
to induce VEGF occur through distinguishable mechanisms. IGF-I increases the cellular content of VEGF mRNA by increasing the
rate of transcription (5-fold after 4 h) and also by increasing the half-life of VEGF mRNA (0.6 ± 0.07 h in control cells
to 2.0 ± 0.37 h in IGF-I-treated cells). Monoclonal antibody (αIR3) directed against the type 1 IGF receptor significantly
attenuated the ability of IGF-I to promote expression of VEGF mRNA. Interestingly, by itself αIR3 acted as a weak agonist
and induced a modest increase in the cellular content of VEGF mRNA. αIR3 also promoted tyrosine phosphorylation of the β subunit
of the IGF-I receptor, and the magnitude of this response was comparable with that induced by IGF-I. These observations point
to a nonlinear relationship between activation of the IGF-I receptor and induction of VEGF mRNA. Thus, in addition to its
direct, growth stimulatory effect on transformed cells, IGF-I induces the expression of VEGF which can promote the progression
of cancer by regulating the development of new blood vessels.</abstract><cop>United States</cop><pub>American Society for Biochemistry and Molecular Biology</pub><pmid>8910616</pmid><doi>10.1074/jbc.271.46.29483</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | The Journal of biological chemistry, 1996-11, Vol.271 (46), p.29483-29488 |
| issn | 0021-9258 1083-351X |
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| source | MEDLINE; Alma/SFX Local Collection; EZB Electronic Journals Library |
| subjects | Colorectal Neoplasms - metabolism Colorectal Neoplasms - pathology Endothelial Growth Factors - biosynthesis Endothelial Growth Factors - genetics Gene Expression Regulation - physiology Humans Insulin-Like Growth Factor I - physiology Lymphokines - biosynthesis Lymphokines - genetics RNA, Messenger - genetics RNA, Messenger - metabolism Vascular Endothelial Growth Factor A Vascular Endothelial Growth Factors |
| title | Induction of Vascular Endothelial Growth Factor by Insulin-like Growth Factor 1 in Colorectal Carcinoma |
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