Up-regulation and co-expression of fibroblast growth factor receptors in human gastric cancer
Fibroblast growth factor (FGF), a key regulatory factor of cell growth and differentiation, is involved in embryonic development, angiogenesis, and tumorigenesis. To date, four different FGF receptors (FGFRs) have been cloned and characterized. We examined the expression of four FGFRs in human gastr...
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| Veröffentlicht in: | Journal of cancer research and clinical oncology 2000-09, Vol.126 (9), p.519-528 |
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| description | Fibroblast growth factor (FGF), a key regulatory factor of cell growth and differentiation, is involved in embryonic development, angiogenesis, and tumorigenesis. To date, four different FGF receptors (FGFRs) have been cloned and characterized. We examined the expression of four FGFRs in human gastric cancer tissues and cell lines using Northern analysis, ribonuclease protection assay, and immunohistochemistry. The mRNAs of FGFR-1 (10/14), FGFR-2 (9/14), and FGFR-4 (9/14) were up-regulated in cancer compared with normal tissues. FGFR-3 mRNAs were barely detectable in both normal and cancer tissues. These FGFR mRNAs were co-expressed in various combinations of two or three in the same tissue. Immunohistochemistry confirmed specific staining of multiple FGFRs, except FGFR-3, in the cancer specimens. To investigate the functional significance of FGFR co-expression we examined the invasive property of SNU-16 cells, which exhibited gene amplification of FGFR-2, -3, and -4 as well as over-expression of keratinocyte growth factor receptor (KGFR), a splice variant of FGFR-2, and FGFR-4 mRNA. KGF plus acidic FGF (aFGF), KGF, and aFGF treatment enhanced the invasive potential of SNU-16 cells over the control by 100%, 107%, and 47%, respectively, indicating that neither additive nor synergistic effect was induced by stimulation with aFGF plus KGF. These results suggest that co-expression of FGFRs in various combinations may cause subtle changes in the progression of gastric cancer. |
| doi_str_mv | 10.1007/s004320000128 |
| format | Article |
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To investigate the functional significance of FGFR co-expression we examined the invasive property of SNU-16 cells, which exhibited gene amplification of FGFR-2, -3, and -4 as well as over-expression of keratinocyte growth factor receptor (KGFR), a splice variant of FGFR-2, and FGFR-4 mRNA. KGF plus acidic FGF (aFGF), KGF, and aFGF treatment enhanced the invasive potential of SNU-16 cells over the control by 100%, 107%, and 47%, respectively, indicating that neither additive nor synergistic effect was induced by stimulation with aFGF plus KGF. These results suggest that co-expression of FGFRs in various combinations may cause subtle changes in the progression of gastric cancer.</description><identifier>ISSN: 0171-5216</identifier><identifier>EISSN: 1432-1335</identifier><identifier>DOI: 10.1007/s004320000128</identifier><identifier>PMID: 11003564</identifier><identifier>CODEN: JCROD7</identifier><language>eng</language><publisher>Berlin: Springer</publisher><subject>Alternative Splicing ; Biological and medical sciences ; Blotting, Northern ; Fibroblast Growth Factor 1 - pharmacology ; Fibroblast Growth Factor 10 ; Fibroblast Growth Factor 7 ; Fibroblast Growth Factors ; Gastroenterology. Liver. Pancreas. Abdomen ; Gene Amplification ; Growth Substances - pharmacology ; Humans ; Immunohistochemistry ; Medical sciences ; Protein Isoforms ; Receptor Protein-Tyrosine Kinases - biosynthesis ; Receptor Protein-Tyrosine Kinases - genetics ; Receptor, Fibroblast Growth Factor, Type 1 ; Receptor, Fibroblast Growth Factor, Type 2 ; Receptors, Fibroblast Growth Factor - biosynthesis ; Receptors, Fibroblast Growth Factor - genetics ; Receptors, Fibroblast Growth Factor - metabolism ; Receptors, Growth Factor - metabolism ; RNA, Messenger - biosynthesis ; RNA, Messenger - genetics ; Stomach Neoplasms - genetics ; Stomach Neoplasms - metabolism ; Stomach. Duodenum. Small intestine. Colon. Rectum. 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C</creatorcontrib><creatorcontrib>KIM, E.-G</creatorcontrib><title>Up-regulation and co-expression of fibroblast growth factor receptors in human gastric cancer</title><title>Journal of cancer research and clinical oncology</title><addtitle>J Cancer Res Clin Oncol</addtitle><description>Fibroblast growth factor (FGF), a key regulatory factor of cell growth and differentiation, is involved in embryonic development, angiogenesis, and tumorigenesis. To date, four different FGF receptors (FGFRs) have been cloned and characterized. We examined the expression of four FGFRs in human gastric cancer tissues and cell lines using Northern analysis, ribonuclease protection assay, and immunohistochemistry. The mRNAs of FGFR-1 (10/14), FGFR-2 (9/14), and FGFR-4 (9/14) were up-regulated in cancer compared with normal tissues. FGFR-3 mRNAs were barely detectable in both normal and cancer tissues. These FGFR mRNAs were co-expressed in various combinations of two or three in the same tissue. Immunohistochemistry confirmed specific staining of multiple FGFRs, except FGFR-3, in the cancer specimens. To investigate the functional significance of FGFR co-expression we examined the invasive property of SNU-16 cells, which exhibited gene amplification of FGFR-2, -3, and -4 as well as over-expression of keratinocyte growth factor receptor (KGFR), a splice variant of FGFR-2, and FGFR-4 mRNA. KGF plus acidic FGF (aFGF), KGF, and aFGF treatment enhanced the invasive potential of SNU-16 cells over the control by 100%, 107%, and 47%, respectively, indicating that neither additive nor synergistic effect was induced by stimulation with aFGF plus KGF. These results suggest that co-expression of FGFRs in various combinations may cause subtle changes in the progression of gastric cancer.</description><subject>Alternative Splicing</subject><subject>Biological and medical sciences</subject><subject>Blotting, Northern</subject><subject>Fibroblast Growth Factor 1 - pharmacology</subject><subject>Fibroblast Growth Factor 10</subject><subject>Fibroblast Growth Factor 7</subject><subject>Fibroblast Growth Factors</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Gene Amplification</subject><subject>Growth Substances - pharmacology</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Medical sciences</subject><subject>Protein Isoforms</subject><subject>Receptor Protein-Tyrosine Kinases - biosynthesis</subject><subject>Receptor Protein-Tyrosine Kinases - genetics</subject><subject>Receptor, Fibroblast Growth Factor, Type 1</subject><subject>Receptor, Fibroblast Growth Factor, Type 2</subject><subject>Receptors, Fibroblast Growth Factor - biosynthesis</subject><subject>Receptors, Fibroblast Growth Factor - genetics</subject><subject>Receptors, Fibroblast Growth Factor - metabolism</subject><subject>Receptors, Growth Factor - metabolism</subject><subject>RNA, Messenger - biosynthesis</subject><subject>RNA, Messenger - genetics</subject><subject>Stomach Neoplasms - genetics</subject><subject>Stomach Neoplasms - metabolism</subject><subject>Stomach. Duodenum. Small intestine. Colon. Rectum. 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Abdomen</topic><topic>Gene Amplification</topic><topic>Growth Substances - pharmacology</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Medical sciences</topic><topic>Protein Isoforms</topic><topic>Receptor Protein-Tyrosine Kinases - biosynthesis</topic><topic>Receptor Protein-Tyrosine Kinases - genetics</topic><topic>Receptor, Fibroblast Growth Factor, Type 1</topic><topic>Receptor, Fibroblast Growth Factor, Type 2</topic><topic>Receptors, Fibroblast Growth Factor - biosynthesis</topic><topic>Receptors, Fibroblast Growth Factor - genetics</topic><topic>Receptors, Fibroblast Growth Factor - metabolism</topic><topic>Receptors, Growth Factor - metabolism</topic><topic>RNA, Messenger - biosynthesis</topic><topic>RNA, Messenger - genetics</topic><topic>Stomach Neoplasms - genetics</topic><topic>Stomach Neoplasms - metabolism</topic><topic>Stomach. Duodenum. Small intestine. Colon. Rectum. 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C</au><au>KIM, E.-G</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Up-regulation and co-expression of fibroblast growth factor receptors in human gastric cancer</atitle><jtitle>Journal of cancer research and clinical oncology</jtitle><addtitle>J Cancer Res Clin Oncol</addtitle><date>2000-09-01</date><risdate>2000</risdate><volume>126</volume><issue>9</issue><spage>519</spage><epage>528</epage><pages>519-528</pages><issn>0171-5216</issn><eissn>1432-1335</eissn><coden>JCROD7</coden><abstract>Fibroblast growth factor (FGF), a key regulatory factor of cell growth and differentiation, is involved in embryonic development, angiogenesis, and tumorigenesis. To date, four different FGF receptors (FGFRs) have been cloned and characterized. We examined the expression of four FGFRs in human gastric cancer tissues and cell lines using Northern analysis, ribonuclease protection assay, and immunohistochemistry. The mRNAs of FGFR-1 (10/14), FGFR-2 (9/14), and FGFR-4 (9/14) were up-regulated in cancer compared with normal tissues. FGFR-3 mRNAs were barely detectable in both normal and cancer tissues. These FGFR mRNAs were co-expressed in various combinations of two or three in the same tissue. Immunohistochemistry confirmed specific staining of multiple FGFRs, except FGFR-3, in the cancer specimens. To investigate the functional significance of FGFR co-expression we examined the invasive property of SNU-16 cells, which exhibited gene amplification of FGFR-2, -3, and -4 as well as over-expression of keratinocyte growth factor receptor (KGFR), a splice variant of FGFR-2, and FGFR-4 mRNA. KGF plus acidic FGF (aFGF), KGF, and aFGF treatment enhanced the invasive potential of SNU-16 cells over the control by 100%, 107%, and 47%, respectively, indicating that neither additive nor synergistic effect was induced by stimulation with aFGF plus KGF. These results suggest that co-expression of FGFRs in various combinations may cause subtle changes in the progression of gastric cancer.</abstract><cop>Berlin</cop><pub>Springer</pub><pmid>11003564</pmid><doi>10.1007/s004320000128</doi><tpages>10</tpages></addata></record> |
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| subjects | Alternative Splicing Biological and medical sciences Blotting, Northern Fibroblast Growth Factor 1 - pharmacology Fibroblast Growth Factor 10 Fibroblast Growth Factor 7 Fibroblast Growth Factors Gastroenterology. Liver. Pancreas. Abdomen Gene Amplification Growth Substances - pharmacology Humans Immunohistochemistry Medical sciences Protein Isoforms Receptor Protein-Tyrosine Kinases - biosynthesis Receptor Protein-Tyrosine Kinases - genetics Receptor, Fibroblast Growth Factor, Type 1 Receptor, Fibroblast Growth Factor, Type 2 Receptors, Fibroblast Growth Factor - biosynthesis Receptors, Fibroblast Growth Factor - genetics Receptors, Fibroblast Growth Factor - metabolism Receptors, Growth Factor - metabolism RNA, Messenger - biosynthesis RNA, Messenger - genetics Stomach Neoplasms - genetics Stomach Neoplasms - metabolism Stomach. Duodenum. Small intestine. Colon. Rectum. Anus Tumors Up-Regulation |
| title | Up-regulation and co-expression of fibroblast growth factor receptors in human gastric cancer |
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