Significance of nerve growth factor overexpression and its autocrine loop in oesophageal squamous cell carcinoma
Nerve growth factor (NGF) is overexpressed not only in nervous system, but also in several types of cancers. However, the role of NGF in oesophageal squamous cell carcinoma (OESCC) remains unclear. Here, we show the first evidence of NGF-TrkA autocrine loop and clinical significance of NGF overexpre...
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| Veröffentlicht in: | British journal of cancer 2006-08, Vol.95 (3), p.322-330 |
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| creator | Tsunoda, S Okumura, T Ito, T Mori, Y Soma, T Watanabe, G Kaganoi, J Itami, A Sakai, Y Shimada, Y |
| description | Nerve growth factor (NGF) is overexpressed not only in nervous system, but also in several types of cancers. However, the role of NGF in oesophageal squamous cell carcinoma (OESCC) remains unclear. Here, we show the first evidence of NGF-TrkA autocrine loop and clinical significance of NGF overexpression in OESCC. Immunohistochemical study of 109 OESCC specimens revealed that NGF overexpression, found in 63 out of 109 patients (57.8%), was associated with lymph node metastasis, distant metastasis, higher TNM stage, poorer tumour differentiation, and poorer survival. NGF overexpression was also associated with strong expression of TrkA and negative expression of low-affinity neurotrophin receptor (p75NTR). Semiquantitative reverse transcription–polymerase chain reaction (RT–PCR) of 19 surgical specimens showed upregulation of NGF mRNA in 17 out of 19 (89%) patients. All five OESCC cell lines tested
in vitro
secreted detectable NGF in enzyme-linked immunosorbent assay, and expressed TrkA and p75NTR on RT–PCR and Western blot. The motility of HSA/c, one of the OESCC cell lines overexpressing NGF, was significantly decreased by either neutralising anti-NGF antibody, an inhibitor of TrkA, or NGF-small interfering RNA in transwell migration assay. Our findings suggest that NGF is of potential interest not only as a prognostic factor, but also as a novel therapeutic target in OESCC. |
| doi_str_mv | 10.1038/sj.bjc.6603255 |
| format | Article |
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in vitro
secreted detectable NGF in enzyme-linked immunosorbent assay, and expressed TrkA and p75NTR on RT–PCR and Western blot. The motility of HSA/c, one of the OESCC cell lines overexpressing NGF, was significantly decreased by either neutralising anti-NGF antibody, an inhibitor of TrkA, or NGF-small interfering RNA in transwell migration assay. Our findings suggest that NGF is of potential interest not only as a prognostic factor, but also as a novel therapeutic target in OESCC.</description><identifier>ISSN: 0007-0920</identifier><identifier>EISSN: 1532-1827</identifier><identifier>DOI: 10.1038/sj.bjc.6603255</identifier><identifier>PMID: 16832412</identifier><identifier>CODEN: BJCAAI</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>Adult ; Aged ; Aged, 80 and over ; Antibodies - pharmacology ; Autocrine Communication - drug effects ; Autocrine Communication - genetics ; Biological and medical sciences ; Biomedical and Life Sciences ; Biomedicine ; Cancer Research ; Carcinoma, Squamous Cell - genetics ; Carcinoma, Squamous Cell - pathology ; Carcinoma, Squamous Cell - surgery ; Cell Line, Tumor ; Cell Movement - drug effects ; Dose-Response Relationship, Drug ; Drug Resistance ; Epidemiology ; Esophageal cancer ; Esophageal Neoplasms - genetics ; Esophageal Neoplasms - pathology ; Esophageal Neoplasms - surgery ; Esophagus ; Female ; Gastroenterology. Liver. Pancreas. Abdomen ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic - drug effects ; Gene Expression Regulation, Neoplastic - genetics ; Growth factors ; Humans ; Kinases ; Lymphatic system ; Male ; Medical prognosis ; Medical research ; Medical sciences ; Metastasis ; Middle Aged ; Molecular Diagnostics ; Molecular Medicine ; Nerve Growth Factor - biosynthesis ; Nerve Growth Factor - drug effects ; Nerve Growth Factor - genetics ; Nervous system ; Oncology ; Receptor, trkA ; Receptors, Nerve Growth Factor - antagonists & inhibitors ; Receptors, Nerve Growth Factor - genetics ; Reverse Transcriptase Polymerase Chain Reaction ; RNA, Small Interfering - pharmacology ; Surgery ; Tumor Cells, Cultured ; Tumors</subject><ispartof>British journal of cancer, 2006-08, Vol.95 (3), p.322-330</ispartof><rights>The Author(s) 2006</rights><rights>2006 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Aug 7, 2006</rights><rights>Copyright © 2006 Cancer Research UK 2006 Cancer Research UK</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c605t-479cf1783e41b1c2f750d2149a96956968ae0f2e1917ff03d8ac4aacfc661b43</citedby><cites>FETCH-LOGICAL-c605t-479cf1783e41b1c2f750d2149a96956968ae0f2e1917ff03d8ac4aacfc661b43</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/PMC2360647/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2360647/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,2727,27924,27925,41488,42557,51319,53791,53793</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18031739$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16832412$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tsunoda, S</creatorcontrib><creatorcontrib>Okumura, T</creatorcontrib><creatorcontrib>Ito, T</creatorcontrib><creatorcontrib>Mori, Y</creatorcontrib><creatorcontrib>Soma, T</creatorcontrib><creatorcontrib>Watanabe, G</creatorcontrib><creatorcontrib>Kaganoi, J</creatorcontrib><creatorcontrib>Itami, A</creatorcontrib><creatorcontrib>Sakai, Y</creatorcontrib><creatorcontrib>Shimada, Y</creatorcontrib><title>Significance of nerve growth factor overexpression and its autocrine loop in oesophageal squamous cell carcinoma</title><title>British journal of cancer</title><addtitle>Br J Cancer</addtitle><addtitle>Br J Cancer</addtitle><description>Nerve growth factor (NGF) is overexpressed not only in nervous system, but also in several types of cancers. However, the role of NGF in oesophageal squamous cell carcinoma (OESCC) remains unclear. Here, we show the first evidence of NGF-TrkA autocrine loop and clinical significance of NGF overexpression in OESCC. Immunohistochemical study of 109 OESCC specimens revealed that NGF overexpression, found in 63 out of 109 patients (57.8%), was associated with lymph node metastasis, distant metastasis, higher TNM stage, poorer tumour differentiation, and poorer survival. NGF overexpression was also associated with strong expression of TrkA and negative expression of low-affinity neurotrophin receptor (p75NTR). Semiquantitative reverse transcription–polymerase chain reaction (RT–PCR) of 19 surgical specimens showed upregulation of NGF mRNA in 17 out of 19 (89%) patients. All five OESCC cell lines tested
in vitro
secreted detectable NGF in enzyme-linked immunosorbent assay, and expressed TrkA and p75NTR on RT–PCR and Western blot. The motility of HSA/c, one of the OESCC cell lines overexpressing NGF, was significantly decreased by either neutralising anti-NGF antibody, an inhibitor of TrkA, or NGF-small interfering RNA in transwell migration assay. Our findings suggest that NGF is of potential interest not only as a prognostic factor, but also as a novel therapeutic target in OESCC.</description><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Antibodies - pharmacology</subject><subject>Autocrine Communication - drug effects</subject><subject>Autocrine Communication - genetics</subject><subject>Biological and medical sciences</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cancer Research</subject><subject>Carcinoma, Squamous Cell - genetics</subject><subject>Carcinoma, Squamous Cell - pathology</subject><subject>Carcinoma, Squamous Cell - surgery</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement - drug effects</subject><subject>Dose-Response Relationship, Drug</subject><subject>Drug Resistance</subject><subject>Epidemiology</subject><subject>Esophageal cancer</subject><subject>Esophageal Neoplasms - genetics</subject><subject>Esophageal Neoplasms - pathology</subject><subject>Esophageal Neoplasms - surgery</subject><subject>Esophagus</subject><subject>Female</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Gene Expression Profiling</subject><subject>Gene Expression Regulation, Neoplastic - drug effects</subject><subject>Gene Expression Regulation, Neoplastic - genetics</subject><subject>Growth factors</subject><subject>Humans</subject><subject>Kinases</subject><subject>Lymphatic system</subject><subject>Male</subject><subject>Medical prognosis</subject><subject>Medical research</subject><subject>Medical sciences</subject><subject>Metastasis</subject><subject>Middle Aged</subject><subject>Molecular Diagnostics</subject><subject>Molecular Medicine</subject><subject>Nerve Growth Factor - biosynthesis</subject><subject>Nerve Growth Factor - drug effects</subject><subject>Nerve Growth Factor - genetics</subject><subject>Nervous system</subject><subject>Oncology</subject><subject>Receptor, trkA</subject><subject>Receptors, Nerve Growth Factor - antagonists & inhibitors</subject><subject>Receptors, Nerve Growth Factor - genetics</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA, Small Interfering - pharmacology</subject><subject>Surgery</subject><subject>Tumor Cells, Cultured</subject><subject>Tumors</subject><issn>0007-0920</issn><issn>1532-1827</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><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>eNp9kctvEzEQxlcIREPhyg1kIQGnTe19-HFBqipeUiUO9G5NnPHG0cbe2rsp_Pd1lKUBJDhZ1vzmm_nmK4qXjC4ZreVF2i5XW7PknNZV2z4qFqytq5LJSjwuFpRSUVJV0bPiWUrb_FVUiqfFGeOyrhpWLYrhu-u8s86AN0iCJR7jHkkXw924IRbMGCIJe4z4Y4iYkguegF8TNyYC0xhMdB5JH8JAnCcBUxg20CH0JN1OsAtTIgb7nhiIxvmwg-fFEwt9whfze17cfPp4c_WlvP72-evV5XVpOG3HshHKWCZkjQ1bMVNZ0dJ1xRoFiquWKy4Bqa2QKSaspfVagmkAjDWcs1VTnxcfjrLDtNrh2qAfI_R6iG4H8acO4PSfFe82ugt7XdWc8kZkgfezQAy3E6ZR71w6WAGP2ZVWbdOKVjUqk-_-S3IpqJINz-Cbv8BtmKLPV8hTKWVMygO0PEImhpQi2oedGdWHyHXa6hy5niPPDa9_d3rC54wz8HYGIBnobcxRu3TiJK2ZqA8-Lo5cyiXfYTyt98_Rr44dHsYp4oPkr_o9d43RFw</recordid><startdate>20060807</startdate><enddate>20060807</enddate><creator>Tsunoda, S</creator><creator>Okumura, T</creator><creator>Ito, T</creator><creator>Mori, Y</creator><creator>Soma, T</creator><creator>Watanabe, G</creator><creator>Kaganoi, J</creator><creator>Itami, A</creator><creator>Sakai, Y</creator><creator>Shimada, Y</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>C6C</scope><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>3V.</scope><scope>7RV</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</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>KB0</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>7TK</scope><scope>5PM</scope></search><sort><creationdate>20060807</creationdate><title>Significance of nerve growth factor overexpression and its autocrine loop in oesophageal squamous cell carcinoma</title><author>Tsunoda, S ; Okumura, T ; Ito, T ; Mori, Y ; Soma, T ; Watanabe, G ; Kaganoi, J ; Itami, A ; Sakai, Y ; Shimada, Y</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c605t-479cf1783e41b1c2f750d2149a96956968ae0f2e1917ff03d8ac4aacfc661b43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Antibodies - pharmacology</topic><topic>Autocrine Communication - drug effects</topic><topic>Autocrine Communication - genetics</topic><topic>Biological and medical sciences</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cancer Research</topic><topic>Carcinoma, Squamous Cell - genetics</topic><topic>Carcinoma, Squamous Cell - pathology</topic><topic>Carcinoma, Squamous Cell - surgery</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement - drug effects</topic><topic>Dose-Response Relationship, Drug</topic><topic>Drug Resistance</topic><topic>Epidemiology</topic><topic>Esophageal cancer</topic><topic>Esophageal Neoplasms - genetics</topic><topic>Esophageal Neoplasms - pathology</topic><topic>Esophageal Neoplasms - surgery</topic><topic>Esophagus</topic><topic>Female</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Gene Expression Profiling</topic><topic>Gene Expression Regulation, Neoplastic - drug effects</topic><topic>Gene Expression Regulation, Neoplastic - genetics</topic><topic>Growth factors</topic><topic>Humans</topic><topic>Kinases</topic><topic>Lymphatic system</topic><topic>Male</topic><topic>Medical prognosis</topic><topic>Medical research</topic><topic>Medical sciences</topic><topic>Metastasis</topic><topic>Middle Aged</topic><topic>Molecular Diagnostics</topic><topic>Molecular Medicine</topic><topic>Nerve Growth Factor - biosynthesis</topic><topic>Nerve Growth Factor - drug effects</topic><topic>Nerve Growth Factor - genetics</topic><topic>Nervous system</topic><topic>Oncology</topic><topic>Receptor, trkA</topic><topic>Receptors, Nerve Growth Factor - antagonists & inhibitors</topic><topic>Receptors, Nerve Growth Factor - genetics</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>RNA, Small Interfering - pharmacology</topic><topic>Surgery</topic><topic>Tumor Cells, Cultured</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tsunoda, S</creatorcontrib><creatorcontrib>Okumura, T</creatorcontrib><creatorcontrib>Ito, T</creatorcontrib><creatorcontrib>Mori, Y</creatorcontrib><creatorcontrib>Soma, T</creatorcontrib><creatorcontrib>Watanabe, G</creatorcontrib><creatorcontrib>Kaganoi, J</creatorcontrib><creatorcontrib>Itami, A</creatorcontrib><creatorcontrib>Sakai, Y</creatorcontrib><creatorcontrib>Shimada, Y</creatorcontrib><collection>Springer Nature OA Free Journals</collection><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 Central (Corporate)</collection><collection>Nursing & Allied Health Database</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>British Nursing Database</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>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Nursing & Allied Health Premium</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>Neurosciences Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>British journal of cancer</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tsunoda, S</au><au>Okumura, T</au><au>Ito, T</au><au>Mori, Y</au><au>Soma, T</au><au>Watanabe, G</au><au>Kaganoi, J</au><au>Itami, A</au><au>Sakai, Y</au><au>Shimada, Y</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Significance of nerve growth factor overexpression and its autocrine loop in oesophageal squamous cell carcinoma</atitle><jtitle>British journal of cancer</jtitle><stitle>Br J Cancer</stitle><addtitle>Br J Cancer</addtitle><date>2006-08-07</date><risdate>2006</risdate><volume>95</volume><issue>3</issue><spage>322</spage><epage>330</epage><pages>322-330</pages><issn>0007-0920</issn><eissn>1532-1827</eissn><coden>BJCAAI</coden><abstract>Nerve growth factor (NGF) is overexpressed not only in nervous system, but also in several types of cancers. However, the role of NGF in oesophageal squamous cell carcinoma (OESCC) remains unclear. Here, we show the first evidence of NGF-TrkA autocrine loop and clinical significance of NGF overexpression in OESCC. Immunohistochemical study of 109 OESCC specimens revealed that NGF overexpression, found in 63 out of 109 patients (57.8%), was associated with lymph node metastasis, distant metastasis, higher TNM stage, poorer tumour differentiation, and poorer survival. NGF overexpression was also associated with strong expression of TrkA and negative expression of low-affinity neurotrophin receptor (p75NTR). Semiquantitative reverse transcription–polymerase chain reaction (RT–PCR) of 19 surgical specimens showed upregulation of NGF mRNA in 17 out of 19 (89%) patients. All five OESCC cell lines tested
in vitro
secreted detectable NGF in enzyme-linked immunosorbent assay, and expressed TrkA and p75NTR on RT–PCR and Western blot. The motility of HSA/c, one of the OESCC cell lines overexpressing NGF, was significantly decreased by either neutralising anti-NGF antibody, an inhibitor of TrkA, or NGF-small interfering RNA in transwell migration assay. Our findings suggest that NGF is of potential interest not only as a prognostic factor, but also as a novel therapeutic target in OESCC.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>16832412</pmid><doi>10.1038/sj.bjc.6603255</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adult Aged Aged, 80 and over Antibodies - pharmacology Autocrine Communication - drug effects Autocrine Communication - genetics Biological and medical sciences Biomedical and Life Sciences Biomedicine Cancer Research Carcinoma, Squamous Cell - genetics Carcinoma, Squamous Cell - pathology Carcinoma, Squamous Cell - surgery Cell Line, Tumor Cell Movement - drug effects Dose-Response Relationship, Drug Drug Resistance Epidemiology Esophageal cancer Esophageal Neoplasms - genetics Esophageal Neoplasms - pathology Esophageal Neoplasms - surgery Esophagus Female Gastroenterology. Liver. Pancreas. Abdomen Gene Expression Profiling Gene Expression Regulation, Neoplastic - drug effects Gene Expression Regulation, Neoplastic - genetics Growth factors Humans Kinases Lymphatic system Male Medical prognosis Medical research Medical sciences Metastasis Middle Aged Molecular Diagnostics Molecular Medicine Nerve Growth Factor - biosynthesis Nerve Growth Factor - drug effects Nerve Growth Factor - genetics Nervous system Oncology Receptor, trkA Receptors, Nerve Growth Factor - antagonists & inhibitors Receptors, Nerve Growth Factor - genetics Reverse Transcriptase Polymerase Chain Reaction RNA, Small Interfering - pharmacology Surgery Tumor Cells, Cultured Tumors |
| title | Significance of nerve growth factor overexpression and its autocrine loop in oesophageal squamous cell carcinoma |
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