Regulatory role of c-Met in insulin-like growth factor-I receptor-mediated migration and invasion of human pancreatic carcinoma cells
Pancreatic carcinoma cells overexpress the insulin-like growth factor-I (IGF-I) receptor (IGF-IR) and the hepatocyte growth factor (HGF) receptor, c-Met, which are both known to mediate tumor cell migration and invasion. We hypothesized that IGF-IR and c-Met cooperate to induce migration and invasio...
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| Veröffentlicht in: | Molecular cancer therapeutics 2006-07, Vol.5 (7), p.1676-1682 |
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| creator | Bauer, Todd W Somcio, Ray J Fan, Fan Liu, Wenbiao Johnson, Marjorie Lesslie, Donald P Evans, Douglas B Gallick, Gary E Ellis, Lee M |
| description | Pancreatic carcinoma cells overexpress the insulin-like growth factor-I (IGF-I) receptor (IGF-IR) and the hepatocyte growth factor (HGF) receptor, c-Met, which are both known to mediate tumor cell migration and invasion. We hypothesized that IGF-IR and c-Met cooperate to induce migration and invasion of human pancreatic carcinoma cells and that IGF-I-mediated migration and invasion depend on c-Met. Migration and invasion assays were done with the human pancreatic cancer cell line L3.6pl treated with PBS, IGF-I, HGF, or IGF-I plus HGF. To determine if c-Met is necessary for IGF-IR-mediated migration and invasion, c-Met was down-regulated in L3.6pl cells via adenoviral infection with a c-Met ribozyme before IGF-I treatment. IGF-I and HGF increased cell migration and invasion. Furthermore, IGF-I plus HGF had a greater than additive effect on cell migration and invasion compared with either growth factor alone. Down-regulation of c-Met nearly completely inhibited IGF-I-mediated migration and invasion. Our findings suggest that IGF-IR and c-Met cooperate to induce migration and invasion of human pancreatic carcinoma cells. Furthermore, c-Met is required for both HGF- and IGF-I-mediated migration and invasion. Elucidation of the signaling pathways that contribute to tumor progression and metastasis should provide a foundation for the development of targeted therapies for pancreatic carcinoma. |
| doi_str_mv | 10.1158/1535-7163.mct-05-0175 |
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We hypothesized that IGF-IR and c-Met cooperate to induce migration and invasion of human pancreatic carcinoma cells and that IGF-I-mediated migration and invasion depend on c-Met. Migration and invasion assays were done with the human pancreatic cancer cell line L3.6pl treated with PBS, IGF-I, HGF, or IGF-I plus HGF. To determine if c-Met is necessary for IGF-IR-mediated migration and invasion, c-Met was down-regulated in L3.6pl cells via adenoviral infection with a c-Met ribozyme before IGF-I treatment. IGF-I and HGF increased cell migration and invasion. Furthermore, IGF-I plus HGF had a greater than additive effect on cell migration and invasion compared with either growth factor alone. Down-regulation of c-Met nearly completely inhibited IGF-I-mediated migration and invasion. Our findings suggest that IGF-IR and c-Met cooperate to induce migration and invasion of human pancreatic carcinoma cells. Furthermore, c-Met is required for both HGF- and IGF-I-mediated migration and invasion. Elucidation of the signaling pathways that contribute to tumor progression and metastasis should provide a foundation for the development of targeted therapies for pancreatic carcinoma.</description><identifier>ISSN: 1535-7163</identifier><identifier>EISSN: 1538-8514</identifier><identifier>DOI: 10.1158/1535-7163.mct-05-0175</identifier><identifier>PMID: 16891453</identifier><language>eng</language><publisher>United States</publisher><subject>Carcinoma - metabolism ; Carcinoma - pathology ; Cell Movement - drug effects ; Hepatocyte Growth Factor - pharmacology ; Humans ; Insulin-Like Growth Factor I - pharmacology ; Neoplasm Invasiveness ; Pancreatic Neoplasms - metabolism ; Pancreatic Neoplasms - pathology ; Phosphorylation ; Proto-Oncogene Proteins c-met - antagonists & inhibitors ; Proto-Oncogene Proteins c-met - metabolism ; Receptor, IGF Type 1 - metabolism</subject><ispartof>Molecular cancer therapeutics, 2006-07, Vol.5 (7), p.1676-1682</ispartof><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c420t-59cd50b054f7ee0a751f0c5d1cc5348a1bb8873562f0d16dfc7151589d7ece0b3</citedby><cites>FETCH-LOGICAL-c420t-59cd50b054f7ee0a751f0c5d1cc5348a1bb8873562f0d16dfc7151589d7ece0b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,3356,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16891453$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bauer, Todd W</creatorcontrib><creatorcontrib>Somcio, Ray J</creatorcontrib><creatorcontrib>Fan, Fan</creatorcontrib><creatorcontrib>Liu, Wenbiao</creatorcontrib><creatorcontrib>Johnson, Marjorie</creatorcontrib><creatorcontrib>Lesslie, Donald P</creatorcontrib><creatorcontrib>Evans, Douglas B</creatorcontrib><creatorcontrib>Gallick, Gary E</creatorcontrib><creatorcontrib>Ellis, Lee M</creatorcontrib><title>Regulatory role of c-Met in insulin-like growth factor-I receptor-mediated migration and invasion of human pancreatic carcinoma cells</title><title>Molecular cancer therapeutics</title><addtitle>Mol Cancer Ther</addtitle><description>Pancreatic carcinoma cells overexpress the insulin-like growth factor-I (IGF-I) receptor (IGF-IR) and the hepatocyte growth factor (HGF) receptor, c-Met, which are both known to mediate tumor cell migration and invasion. We hypothesized that IGF-IR and c-Met cooperate to induce migration and invasion of human pancreatic carcinoma cells and that IGF-I-mediated migration and invasion depend on c-Met. Migration and invasion assays were done with the human pancreatic cancer cell line L3.6pl treated with PBS, IGF-I, HGF, or IGF-I plus HGF. To determine if c-Met is necessary for IGF-IR-mediated migration and invasion, c-Met was down-regulated in L3.6pl cells via adenoviral infection with a c-Met ribozyme before IGF-I treatment. IGF-I and HGF increased cell migration and invasion. Furthermore, IGF-I plus HGF had a greater than additive effect on cell migration and invasion compared with either growth factor alone. Down-regulation of c-Met nearly completely inhibited IGF-I-mediated migration and invasion. Our findings suggest that IGF-IR and c-Met cooperate to induce migration and invasion of human pancreatic carcinoma cells. Furthermore, c-Met is required for both HGF- and IGF-I-mediated migration and invasion. Elucidation of the signaling pathways that contribute to tumor progression and metastasis should provide a foundation for the development of targeted therapies for pancreatic carcinoma.</description><subject>Carcinoma - metabolism</subject><subject>Carcinoma - pathology</subject><subject>Cell Movement - drug effects</subject><subject>Hepatocyte Growth Factor - pharmacology</subject><subject>Humans</subject><subject>Insulin-Like Growth Factor I - pharmacology</subject><subject>Neoplasm Invasiveness</subject><subject>Pancreatic Neoplasms - metabolism</subject><subject>Pancreatic Neoplasms - pathology</subject><subject>Phosphorylation</subject><subject>Proto-Oncogene Proteins c-met - antagonists & inhibitors</subject><subject>Proto-Oncogene Proteins c-met - metabolism</subject><subject>Receptor, IGF Type 1 - metabolism</subject><issn>1535-7163</issn><issn>1538-8514</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkN9KwzAUh4MoOqePoOTKu2jO2tNklzL8Bw5B9DqkaTqjbTOTVtkD-N6mbiAEchK-3zmHj5Az4JcAKK8AM2QCiuyyNT3jyDgI3COT9C-ZRMj3_-otc0SOY3znHOR8BofkCAo5hxyzCfl5tquh0b0PGxp8Y6mvqWFL21PXpROHxnWscR-WroL_7t9orU2C2QMN1tj1WLa2crq3FW3dKuje-Y7qrkrhLx3HR-r4NrS6o2vdmWATYajRwbjOt5oa2zTxhBzUuon2dHdPyevtzcvinj0-3T0srh-ZyWe8Zzg3FfKSY14La7kWCDU3WIExmOVSQ1lKKTIsZjWvoKhqIwCTrHkl0rK8zKbkYtt3HfznYGOvWhfHDXRn_RBVIQUICTyBuAVN8DEGW6t1cK0OGwVcjf7V6FaNbtVy8aI4qtF_yp3vBgxl8vKf2gnPfgGhK4Qm</recordid><startdate>200607</startdate><enddate>200607</enddate><creator>Bauer, Todd W</creator><creator>Somcio, Ray J</creator><creator>Fan, Fan</creator><creator>Liu, Wenbiao</creator><creator>Johnson, Marjorie</creator><creator>Lesslie, Donald P</creator><creator>Evans, Douglas B</creator><creator>Gallick, Gary E</creator><creator>Ellis, Lee M</creator><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>7X8</scope></search><sort><creationdate>200607</creationdate><title>Regulatory role of c-Met in insulin-like growth factor-I receptor-mediated migration and invasion of human pancreatic carcinoma cells</title><author>Bauer, Todd W ; 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We hypothesized that IGF-IR and c-Met cooperate to induce migration and invasion of human pancreatic carcinoma cells and that IGF-I-mediated migration and invasion depend on c-Met. Migration and invasion assays were done with the human pancreatic cancer cell line L3.6pl treated with PBS, IGF-I, HGF, or IGF-I plus HGF. To determine if c-Met is necessary for IGF-IR-mediated migration and invasion, c-Met was down-regulated in L3.6pl cells via adenoviral infection with a c-Met ribozyme before IGF-I treatment. IGF-I and HGF increased cell migration and invasion. Furthermore, IGF-I plus HGF had a greater than additive effect on cell migration and invasion compared with either growth factor alone. Down-regulation of c-Met nearly completely inhibited IGF-I-mediated migration and invasion. Our findings suggest that IGF-IR and c-Met cooperate to induce migration and invasion of human pancreatic carcinoma cells. 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| subjects | Carcinoma - metabolism Carcinoma - pathology Cell Movement - drug effects Hepatocyte Growth Factor - pharmacology Humans Insulin-Like Growth Factor I - pharmacology Neoplasm Invasiveness Pancreatic Neoplasms - metabolism Pancreatic Neoplasms - pathology Phosphorylation Proto-Oncogene Proteins c-met - antagonists & inhibitors Proto-Oncogene Proteins c-met - metabolism Receptor, IGF Type 1 - metabolism |
| title | Regulatory role of c-Met in insulin-like growth factor-I receptor-mediated migration and invasion of human pancreatic carcinoma cells |
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