Activation of c‐Met (hepatocyte growth factor receptor) in human gastric cancer tissue
c‐Met is a high‐affinity receptor for hepatocyte growth factor (HGF) and plays a crucial role in embryonic development, as well as in the process of tissue repair. Overexpression and amplification of c‐Met are often observed in various cancer tissues, especially in gastric carcinoma. It has, however...
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| Veröffentlicht in: | Cancer science 2004-10, Vol.95 (10), p.803-809 |
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| creator | Inoue, Takao Kataoka, Hiroaki Goto, Kouichiro Nagaike, Koki Igami, Ko Naka, Daiji Kitamura, Naomi Miyazawa, Keiji |
| description | c‐Met is a high‐affinity receptor for hepatocyte growth factor (HGF) and plays a crucial role in embryonic development, as well as in the process of tissue repair. Overexpression and amplification of c‐Met are often observed in various cancer tissues, especially in gastric carcinoma. It has, however, been unclear whether the overexpression leads to activation of the c‐Met receptor. To address this point, we prepared an antibody (anti‐phospho‐Met) which specifically recognizes c‐Met that is phosphorylated at Y1235, a major phosphorylation site of c‐Met. Normal as well as cancerous gastric tissue was positive for anti‐total‐Met staining, whereas only cancerous tissue was strongly positive for anti‐phospho‐Met staining; cells near the basal layer were moderately positive, and the proliferative zone in normal tissue was only weakly positive. Among cancerous tissues from seven patients examined in the present study, those from six patients were strongly positive for phospho‐Met staining. These results indicate that c‐Met is actually activated in gastric carcinoma tissue, and may trigger proliferation/anti‐apoptotic signals. |
| doi_str_mv | 10.1111/j.1349-7006.2004.tb02185.x |
| format | Article |
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Overexpression and amplification of c‐Met are often observed in various cancer tissues, especially in gastric carcinoma. It has, however, been unclear whether the overexpression leads to activation of the c‐Met receptor. To address this point, we prepared an antibody (anti‐phospho‐Met) which specifically recognizes c‐Met that is phosphorylated at Y1235, a major phosphorylation site of c‐Met. Normal as well as cancerous gastric tissue was positive for anti‐total‐Met staining, whereas only cancerous tissue was strongly positive for anti‐phospho‐Met staining; cells near the basal layer were moderately positive, and the proliferative zone in normal tissue was only weakly positive. Among cancerous tissues from seven patients examined in the present study, those from six patients were strongly positive for phospho‐Met staining. These results indicate that c‐Met is actually activated in gastric carcinoma tissue, and may trigger proliferation/anti‐apoptotic signals.</description><identifier>ISSN: 1347-9032</identifier><identifier>EISSN: 1349-7006</identifier><identifier>DOI: 10.1111/j.1349-7006.2004.tb02185.x</identifier><identifier>PMID: 15504247</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Adenocarcinoma - metabolism ; Antibodies, Neoplasm - immunology ; Apoptosis ; Biological and medical sciences ; c-Met protein ; Embryogenesis ; Enzyme Activation ; Gastric cancer ; Gastric Mucosa - metabolism ; Gastroenterology. Liver. Pancreas. Abdomen ; Growth factors ; Hepatocyte growth factor ; Humans ; Immunohistochemistry ; Medical sciences ; Phosphorylation ; Proto-Oncogene Proteins c-met - biosynthesis ; Proto-Oncogene Proteins c-met - immunology ; Stomach Neoplasms - metabolism ; Stomach. Duodenum. Small intestine. Colon. Rectum. Anus ; Tumors</subject><ispartof>Cancer science, 2004-10, Vol.95 (10), p.803-809</ispartof><rights>2005 INIST-CNRS</rights><rights>Copyright John Wiley & Sons, Inc. Oct 2004</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c6473-ba007e1b9e6be084e91645f6c2dc89123621298cd3ed2e1a9f3c980b1f43877c3</citedby><cites>FETCH-LOGICAL-c6473-ba007e1b9e6be084e91645f6c2dc89123621298cd3ed2e1a9f3c980b1f43877c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11158965/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11158965/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,1417,11562,27924,27925,45574,45575,46052,46476,53791,53793</link.rule.ids><linktorsrc>$$Uhttps://onlinelibrary.wiley.com/doi/abs/10.1111%2Fj.1349-7006.2004.tb02185.x$$EView_record_in_Wiley-Blackwell$$FView_record_in_$$GWiley-Blackwell</linktorsrc><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16296756$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15504247$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Inoue, Takao</creatorcontrib><creatorcontrib>Kataoka, Hiroaki</creatorcontrib><creatorcontrib>Goto, Kouichiro</creatorcontrib><creatorcontrib>Nagaike, Koki</creatorcontrib><creatorcontrib>Igami, Ko</creatorcontrib><creatorcontrib>Naka, Daiji</creatorcontrib><creatorcontrib>Kitamura, Naomi</creatorcontrib><creatorcontrib>Miyazawa, Keiji</creatorcontrib><title>Activation of c‐Met (hepatocyte growth factor receptor) in human gastric cancer tissue</title><title>Cancer science</title><addtitle>Cancer Sci</addtitle><description>c‐Met is a high‐affinity receptor for hepatocyte growth factor (HGF) and plays a crucial role in embryonic development, as well as in the process of tissue repair. Overexpression and amplification of c‐Met are often observed in various cancer tissues, especially in gastric carcinoma. It has, however, been unclear whether the overexpression leads to activation of the c‐Met receptor. To address this point, we prepared an antibody (anti‐phospho‐Met) which specifically recognizes c‐Met that is phosphorylated at Y1235, a major phosphorylation site of c‐Met. Normal as well as cancerous gastric tissue was positive for anti‐total‐Met staining, whereas only cancerous tissue was strongly positive for anti‐phospho‐Met staining; cells near the basal layer were moderately positive, and the proliferative zone in normal tissue was only weakly positive. Among cancerous tissues from seven patients examined in the present study, those from six patients were strongly positive for phospho‐Met staining. These results indicate that c‐Met is actually activated in gastric carcinoma tissue, and may trigger proliferation/anti‐apoptotic signals.</description><subject>Adenocarcinoma - metabolism</subject><subject>Antibodies, Neoplasm - immunology</subject><subject>Apoptosis</subject><subject>Biological and medical sciences</subject><subject>c-Met protein</subject><subject>Embryogenesis</subject><subject>Enzyme Activation</subject><subject>Gastric cancer</subject><subject>Gastric Mucosa - metabolism</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Growth factors</subject><subject>Hepatocyte growth factor</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Medical sciences</subject><subject>Phosphorylation</subject><subject>Proto-Oncogene Proteins c-met - biosynthesis</subject><subject>Proto-Oncogene Proteins c-met - immunology</subject><subject>Stomach Neoplasms - metabolism</subject><subject>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</subject><subject>Tumors</subject><issn>1347-9032</issn><issn>1349-7006</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</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>eNqVkc2O0zAQxyMEYj_gFZAFYgWHFH_FsTmAqoovaREHQOJmOe6kdZXGXdvZ3d54BJ6RJ8Gh0S5wYy4eaX7z98z8i-IxwTOS48VmRhhXZY2xmFGM-Sw1mBJZza7vFMc3pbu_87pUmNGj4iTGDcZMcMXvF0ekqjCnvD4uvs1tcpcmOd8j3yL78_uPj5DQszXsTPJ2nwCtgr9Ka9Qam3xAASzscvIcuR6th63p0crEFJxF1vQWAkouxgEeFPda00V4OL2nxde3b74s3pfnn959WMzPSyt4zcrGYFwDaRSIBrDkoIjgVSssXVqpCGWCEqqkXTJYUiBGtcwqiRvScibr2rLT4vVBdzc0W1ha6FMwnd4FtzVhr71x-u9K79Z65S91vmQllaiywtmkEPzFADHprYsWus704IeoxXhNhmUGn_wDbvwQ-rydpkzlkEKOci8PlA0-xgDtzSwEj58SvdGjSXqU1aN_evJPX-fmR39uc9s6GZaBpxNgojVdG_LNXbzlBFWirkTmXh24K9fB_j9G0Iv5Z4kZ-wVG7rkN</recordid><startdate>200410</startdate><enddate>200410</enddate><creator>Inoue, Takao</creator><creator>Kataoka, Hiroaki</creator><creator>Goto, Kouichiro</creator><creator>Nagaike, Koki</creator><creator>Igami, Ko</creator><creator>Naka, Daiji</creator><creator>Kitamura, Naomi</creator><creator>Miyazawa, Keiji</creator><general>Blackwell Publishing Ltd</general><general>Blackwell</general><general>John Wiley & Sons, Inc</general><scope>IQODW</scope><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>8FE</scope><scope>8FH</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>LK8</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>200410</creationdate><title>Activation of c‐Met (hepatocyte growth factor receptor) in human gastric cancer tissue</title><author>Inoue, Takao ; Kataoka, Hiroaki ; Goto, Kouichiro ; Nagaike, Koki ; Igami, Ko ; Naka, Daiji ; Kitamura, Naomi ; Miyazawa, Keiji</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c6473-ba007e1b9e6be084e91645f6c2dc89123621298cd3ed2e1a9f3c980b1f43877c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Adenocarcinoma - metabolism</topic><topic>Antibodies, Neoplasm - immunology</topic><topic>Apoptosis</topic><topic>Biological and medical sciences</topic><topic>c-Met protein</topic><topic>Embryogenesis</topic><topic>Enzyme Activation</topic><topic>Gastric cancer</topic><topic>Gastric Mucosa - metabolism</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Growth factors</topic><topic>Hepatocyte growth factor</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Medical sciences</topic><topic>Phosphorylation</topic><topic>Proto-Oncogene Proteins c-met - biosynthesis</topic><topic>Proto-Oncogene Proteins c-met - immunology</topic><topic>Stomach Neoplasms - metabolism</topic><topic>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Inoue, Takao</creatorcontrib><creatorcontrib>Kataoka, Hiroaki</creatorcontrib><creatorcontrib>Goto, Kouichiro</creatorcontrib><creatorcontrib>Nagaike, Koki</creatorcontrib><creatorcontrib>Igami, Ko</creatorcontrib><creatorcontrib>Naka, Daiji</creatorcontrib><creatorcontrib>Kitamura, Naomi</creatorcontrib><creatorcontrib>Miyazawa, Keiji</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Biological Science Database</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cancer science</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext_linktorsrc</fulltext></delivery><addata><au>Inoue, Takao</au><au>Kataoka, Hiroaki</au><au>Goto, Kouichiro</au><au>Nagaike, Koki</au><au>Igami, Ko</au><au>Naka, Daiji</au><au>Kitamura, Naomi</au><au>Miyazawa, Keiji</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Activation of c‐Met (hepatocyte growth factor receptor) in human gastric cancer tissue</atitle><jtitle>Cancer science</jtitle><addtitle>Cancer Sci</addtitle><date>2004-10</date><risdate>2004</risdate><volume>95</volume><issue>10</issue><spage>803</spage><epage>809</epage><pages>803-809</pages><issn>1347-9032</issn><eissn>1349-7006</eissn><abstract>c‐Met is a high‐affinity receptor for hepatocyte growth factor (HGF) and plays a crucial role in embryonic development, as well as in the process of tissue repair. Overexpression and amplification of c‐Met are often observed in various cancer tissues, especially in gastric carcinoma. It has, however, been unclear whether the overexpression leads to activation of the c‐Met receptor. To address this point, we prepared an antibody (anti‐phospho‐Met) which specifically recognizes c‐Met that is phosphorylated at Y1235, a major phosphorylation site of c‐Met. Normal as well as cancerous gastric tissue was positive for anti‐total‐Met staining, whereas only cancerous tissue was strongly positive for anti‐phospho‐Met staining; cells near the basal layer were moderately positive, and the proliferative zone in normal tissue was only weakly positive. Among cancerous tissues from seven patients examined in the present study, those from six patients were strongly positive for phospho‐Met staining. These results indicate that c‐Met is actually activated in gastric carcinoma tissue, and may trigger proliferation/anti‐apoptotic signals.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>15504247</pmid><doi>10.1111/j.1349-7006.2004.tb02185.x</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adenocarcinoma - metabolism Antibodies, Neoplasm - immunology Apoptosis Biological and medical sciences c-Met protein Embryogenesis Enzyme Activation Gastric cancer Gastric Mucosa - metabolism Gastroenterology. Liver. Pancreas. Abdomen Growth factors Hepatocyte growth factor Humans Immunohistochemistry Medical sciences Phosphorylation Proto-Oncogene Proteins c-met - biosynthesis Proto-Oncogene Proteins c-met - immunology Stomach Neoplasms - metabolism Stomach. Duodenum. Small intestine. Colon. Rectum. Anus Tumors |
| title | Activation of c‐Met (hepatocyte growth factor receptor) in human gastric cancer tissue |
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