NK4, an HGF antagonist, prevents hematogenous pulmonary metastasis by inhibiting adhesion of CT26 cells to endothelial cells
Abstract Hepatocyte growth factor (HGF) plays a definitive role in invasive, angiogenic, and metastatic activities of tumor cells by binding to the c-Met receptor. NK4, a competitive antagonist for HGF and the c-Met receptor, prevents tumor cell growth and metastasis via its bifunctional properties...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Kubota, Takeshi [verfasserIn] Taiyoh, Hiroaki [verfasserIn] Matsumura, Atsushi [verfasserIn] Murayama, Yasutoshi [verfasserIn] Ichikawa, Daisuke [verfasserIn] Okamoto, Kazuma [verfasserIn] Fujiwara, Hitoshi [verfasserIn] Ikoma, Hisashi [verfasserIn] Nakanishi, Masayoshi [verfasserIn] Kikuchi, Shojiro [verfasserIn] Sakakura, Chouhei [verfasserIn] Ochiai, Toshiya [verfasserIn] Kokuba, Yukihito [verfasserIn] Taniguchi, Hiroki [verfasserIn] Sonoyama, Teruhisa [verfasserIn] Matsumoto, Kunio [verfasserIn] Nakamura, Toshikazu [verfasserIn] Otsuji, Eigo [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2009 |
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| Schlagwörter: |
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| Übergeordnetes Werk: |
Enthalten in: Clinical & experimental metastasis - Dordrecht : Springer Science + Business Media B.V., 1983, 26(2009), 5 vom: 21. Feb., Seite 447-456 |
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| Übergeordnetes Werk: |
volume:26 ; year:2009 ; number:5 ; day:21 ; month:02 ; pages:447-456 |
| Links: |
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| DOI / URN: |
10.1007/s10585-009-9244-0 |
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| Katalog-ID: |
SPR011488808 |
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| 100 | 1 | |a Kubota, Takeshi |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a NK4, an HGF antagonist, prevents hematogenous pulmonary metastasis by inhibiting adhesion of CT26 cells to endothelial cells |
| 264 | 1 | |c 2009 | |
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| 337 | |a Computermedien |b c |2 rdamedia | ||
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| 520 | |a Abstract Hepatocyte growth factor (HGF) plays a definitive role in invasive, angiogenic, and metastatic activities of tumor cells by binding to the c-Met receptor. NK4, a competitive antagonist for HGF and the c-Met receptor, prevents tumor cell growth and metastasis via its bifunctional properties to act as an HGF antagonist and angiogenesis inhibitor. In the present study, we investigated the inhibitory effectiveness of NK4 on hematogenous pulmonary metastasis of the CT26 murine colon cancer cell line, focusing on tumor cell adhesion to endothelial cells. In an in vitro adhesion assay, HGF facilitated adhesion of CT26 cells to a murine endothelial cell line (F-2) in a dose-dependent manner. Furthermore, the enhancing effect of HGF on CT26-F-2 cell interaction was blocked by NK4 as well as by anti-HGF antibody. Similarly, HGF-induced phosphorylation of focal adhesion kinase (FAK), downstream of integrin signaling, was reduced by NK4 and by anti-HGF antibody. However, distinct integrin expression on the surface of CT26 cells was not altered by HGF. In an in vivo experimental pulmonary metastasis assay, stable NK4 expression potently decreased the number of pulmonary metastatic foci. The NK4-induced suppression of pulmonary metastasis was partially reversed when HGF was intraperitoneally administered in an adhesive phase. These results suggest that NK4 could act on tumor cells to inhibit CT26 adhesion to endothelial cells by reducing FAK phosphorylation, which is regulated by inside-out HGF/c-Met signaling, and thereby suppress hematogenous pulmonary metastasis. | ||
| 650 | 4 | |a HGF |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a c-Met |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a NK4 |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a CT26 |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Pulmonary metastasis |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Endothelial cell |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a FAK |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Taiyoh, Hiroaki |e verfasserin |4 aut | |
| 700 | 1 | |a Matsumura, Atsushi |e verfasserin |4 aut | |
| 700 | 1 | |a Murayama, Yasutoshi |e verfasserin |4 aut | |
| 700 | 1 | |a Ichikawa, Daisuke |e verfasserin |4 aut | |
| 700 | 1 | |a Okamoto, Kazuma |e verfasserin |4 aut | |
| 700 | 1 | |a Fujiwara, Hitoshi |e verfasserin |4 aut | |
| 700 | 1 | |a Ikoma, Hisashi |e verfasserin |4 aut | |
| 700 | 1 | |a Nakanishi, Masayoshi |e verfasserin |4 aut | |
| 700 | 1 | |a Kikuchi, Shojiro |e verfasserin |4 aut | |
| 700 | 1 | |a Sakakura, Chouhei |e verfasserin |4 aut | |
| 700 | 1 | |a Ochiai, Toshiya |e verfasserin |4 aut | |
| 700 | 1 | |a Kokuba, Yukihito |e verfasserin |4 aut | |
| 700 | 1 | |a Taniguchi, Hiroki |e verfasserin |4 aut | |
| 700 | 1 | |a Sonoyama, Teruhisa |e verfasserin |4 aut | |
| 700 | 1 | |a Matsumoto, Kunio |e verfasserin |4 aut | |
| 700 | 1 | |a Nakamura, Toshikazu |e verfasserin |4 aut | |
| 700 | 1 | |a Otsuji, Eigo |e verfasserin |4 aut | |
| 773 | 0 | 8 | |i Enthalten in |t Clinical & experimental metastasis |d Dordrecht : Springer Science + Business Media B.V., 1983 |g 26(2009), 5 vom: 21. Feb., Seite 447-456 |w (DE-627)306354683 |w (DE-600)1496876-9 |x 1573-7276 |7 nnns |
| 773 | 1 | 8 | |g volume:26 |g year:2009 |g number:5 |g day:21 |g month:02 |g pages:447-456 |
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| 912 | |a GBV_ILN_2011 | ||
| 912 | |a GBV_ILN_2014 | ||
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| 912 | |a GBV_ILN_2037 | ||
| 912 | |a GBV_ILN_2038 | ||
| 912 | |a GBV_ILN_2039 | ||
| 912 | |a GBV_ILN_2044 | ||
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| 912 | |a GBV_ILN_2055 | ||
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| 912 | |a GBV_ILN_2059 | ||
| 912 | |a GBV_ILN_2061 | ||
| 912 | |a GBV_ILN_2064 | ||
| 912 | |a GBV_ILN_2065 | ||
| 912 | |a GBV_ILN_2068 | ||
| 912 | |a GBV_ILN_2070 | ||
| 912 | |a GBV_ILN_2086 | ||
| 912 | |a GBV_ILN_2088 | ||
| 912 | |a GBV_ILN_2093 | ||
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| 912 | |a GBV_ILN_2107 | ||
| 912 | |a GBV_ILN_2108 | ||
| 912 | |a GBV_ILN_2110 | ||
| 912 | |a GBV_ILN_2111 | ||
| 912 | |a GBV_ILN_2112 | ||
| 912 | |a GBV_ILN_2113 | ||
| 912 | |a GBV_ILN_2116 | ||
| 912 | |a GBV_ILN_2118 | ||
| 912 | |a GBV_ILN_2119 | ||
| 912 | |a GBV_ILN_2122 | ||
| 912 | |a GBV_ILN_2129 | ||
| 912 | |a GBV_ILN_2143 | ||
| 912 | |a GBV_ILN_2144 | ||
| 912 | |a GBV_ILN_2147 | ||
| 912 | |a GBV_ILN_2148 | ||
| 912 | |a GBV_ILN_2152 | ||
| 912 | |a GBV_ILN_2153 | ||
| 912 | |a GBV_ILN_2188 | ||
| 912 | |a GBV_ILN_2190 | ||
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| 912 | |a GBV_ILN_2336 | ||
| 912 | |a GBV_ILN_2446 | ||
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| 912 | |a GBV_ILN_4035 | ||
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| 912 | |a GBV_ILN_4112 | ||
| 912 | |a GBV_ILN_4125 | ||
| 912 | |a GBV_ILN_4126 | ||
| 912 | |a GBV_ILN_4242 | ||
| 912 | |a GBV_ILN_4246 | ||
| 912 | |a GBV_ILN_4249 | ||
| 912 | |a GBV_ILN_4251 | ||
| 912 | |a GBV_ILN_4305 | ||
| 912 | |a GBV_ILN_4306 | ||
| 912 | |a GBV_ILN_4307 | ||
| 912 | |a GBV_ILN_4313 | ||
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| 912 | |a GBV_ILN_4323 | ||
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10.1007/s10585-009-9244-0 doi (DE-627)SPR011488808 (SPR)s10585-009-9244-0-e DE-627 ger DE-627 rakwb eng 610 ASE 44.81 bkl Kubota, Takeshi verfasserin aut NK4, an HGF antagonist, prevents hematogenous pulmonary metastasis by inhibiting adhesion of CT26 cells to endothelial cells 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Hepatocyte growth factor (HGF) plays a definitive role in invasive, angiogenic, and metastatic activities of tumor cells by binding to the c-Met receptor. NK4, a competitive antagonist for HGF and the c-Met receptor, prevents tumor cell growth and metastasis via its bifunctional properties to act as an HGF antagonist and angiogenesis inhibitor. In the present study, we investigated the inhibitory effectiveness of NK4 on hematogenous pulmonary metastasis of the CT26 murine colon cancer cell line, focusing on tumor cell adhesion to endothelial cells. In an in vitro adhesion assay, HGF facilitated adhesion of CT26 cells to a murine endothelial cell line (F-2) in a dose-dependent manner. Furthermore, the enhancing effect of HGF on CT26-F-2 cell interaction was blocked by NK4 as well as by anti-HGF antibody. Similarly, HGF-induced phosphorylation of focal adhesion kinase (FAK), downstream of integrin signaling, was reduced by NK4 and by anti-HGF antibody. However, distinct integrin expression on the surface of CT26 cells was not altered by HGF. In an in vivo experimental pulmonary metastasis assay, stable NK4 expression potently decreased the number of pulmonary metastatic foci. The NK4-induced suppression of pulmonary metastasis was partially reversed when HGF was intraperitoneally administered in an adhesive phase. These results suggest that NK4 could act on tumor cells to inhibit CT26 adhesion to endothelial cells by reducing FAK phosphorylation, which is regulated by inside-out HGF/c-Met signaling, and thereby suppress hematogenous pulmonary metastasis. HGF (dpeaa)DE-He213 c-Met (dpeaa)DE-He213 NK4 (dpeaa)DE-He213 CT26 (dpeaa)DE-He213 Pulmonary metastasis (dpeaa)DE-He213 Endothelial cell (dpeaa)DE-He213 FAK (dpeaa)DE-He213 Taiyoh, Hiroaki verfasserin aut Matsumura, Atsushi verfasserin aut Murayama, Yasutoshi verfasserin aut Ichikawa, Daisuke verfasserin aut Okamoto, Kazuma verfasserin aut Fujiwara, Hitoshi verfasserin aut Ikoma, Hisashi verfasserin aut Nakanishi, Masayoshi verfasserin aut Kikuchi, Shojiro verfasserin aut Sakakura, Chouhei verfasserin aut Ochiai, Toshiya verfasserin aut Kokuba, Yukihito verfasserin aut Taniguchi, Hiroki verfasserin aut Sonoyama, Teruhisa verfasserin aut Matsumoto, Kunio verfasserin aut Nakamura, Toshikazu verfasserin aut Otsuji, Eigo verfasserin aut Enthalten in Clinical & experimental metastasis Dordrecht : Springer Science + Business Media B.V., 1983 26(2009), 5 vom: 21. Feb., Seite 447-456 (DE-627)306354683 (DE-600)1496876-9 1573-7276 nnns volume:26 year:2009 number:5 day:21 month:02 pages:447-456 https://dx.doi.org/10.1007/s10585-009-9244-0 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.81 ASE AR 26 2009 5 21 02 447-456 |
| spelling |
10.1007/s10585-009-9244-0 doi (DE-627)SPR011488808 (SPR)s10585-009-9244-0-e DE-627 ger DE-627 rakwb eng 610 ASE 44.81 bkl Kubota, Takeshi verfasserin aut NK4, an HGF antagonist, prevents hematogenous pulmonary metastasis by inhibiting adhesion of CT26 cells to endothelial cells 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Hepatocyte growth factor (HGF) plays a definitive role in invasive, angiogenic, and metastatic activities of tumor cells by binding to the c-Met receptor. NK4, a competitive antagonist for HGF and the c-Met receptor, prevents tumor cell growth and metastasis via its bifunctional properties to act as an HGF antagonist and angiogenesis inhibitor. In the present study, we investigated the inhibitory effectiveness of NK4 on hematogenous pulmonary metastasis of the CT26 murine colon cancer cell line, focusing on tumor cell adhesion to endothelial cells. In an in vitro adhesion assay, HGF facilitated adhesion of CT26 cells to a murine endothelial cell line (F-2) in a dose-dependent manner. Furthermore, the enhancing effect of HGF on CT26-F-2 cell interaction was blocked by NK4 as well as by anti-HGF antibody. Similarly, HGF-induced phosphorylation of focal adhesion kinase (FAK), downstream of integrin signaling, was reduced by NK4 and by anti-HGF antibody. However, distinct integrin expression on the surface of CT26 cells was not altered by HGF. In an in vivo experimental pulmonary metastasis assay, stable NK4 expression potently decreased the number of pulmonary metastatic foci. The NK4-induced suppression of pulmonary metastasis was partially reversed when HGF was intraperitoneally administered in an adhesive phase. These results suggest that NK4 could act on tumor cells to inhibit CT26 adhesion to endothelial cells by reducing FAK phosphorylation, which is regulated by inside-out HGF/c-Met signaling, and thereby suppress hematogenous pulmonary metastasis. HGF (dpeaa)DE-He213 c-Met (dpeaa)DE-He213 NK4 (dpeaa)DE-He213 CT26 (dpeaa)DE-He213 Pulmonary metastasis (dpeaa)DE-He213 Endothelial cell (dpeaa)DE-He213 FAK (dpeaa)DE-He213 Taiyoh, Hiroaki verfasserin aut Matsumura, Atsushi verfasserin aut Murayama, Yasutoshi verfasserin aut Ichikawa, Daisuke verfasserin aut Okamoto, Kazuma verfasserin aut Fujiwara, Hitoshi verfasserin aut Ikoma, Hisashi verfasserin aut Nakanishi, Masayoshi verfasserin aut Kikuchi, Shojiro verfasserin aut Sakakura, Chouhei verfasserin aut Ochiai, Toshiya verfasserin aut Kokuba, Yukihito verfasserin aut Taniguchi, Hiroki verfasserin aut Sonoyama, Teruhisa verfasserin aut Matsumoto, Kunio verfasserin aut Nakamura, Toshikazu verfasserin aut Otsuji, Eigo verfasserin aut Enthalten in Clinical & experimental metastasis Dordrecht : Springer Science + Business Media B.V., 1983 26(2009), 5 vom: 21. Feb., Seite 447-456 (DE-627)306354683 (DE-600)1496876-9 1573-7276 nnns volume:26 year:2009 number:5 day:21 month:02 pages:447-456 https://dx.doi.org/10.1007/s10585-009-9244-0 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.81 ASE AR 26 2009 5 21 02 447-456 |
| allfields_unstemmed |
10.1007/s10585-009-9244-0 doi (DE-627)SPR011488808 (SPR)s10585-009-9244-0-e DE-627 ger DE-627 rakwb eng 610 ASE 44.81 bkl Kubota, Takeshi verfasserin aut NK4, an HGF antagonist, prevents hematogenous pulmonary metastasis by inhibiting adhesion of CT26 cells to endothelial cells 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Hepatocyte growth factor (HGF) plays a definitive role in invasive, angiogenic, and metastatic activities of tumor cells by binding to the c-Met receptor. NK4, a competitive antagonist for HGF and the c-Met receptor, prevents tumor cell growth and metastasis via its bifunctional properties to act as an HGF antagonist and angiogenesis inhibitor. In the present study, we investigated the inhibitory effectiveness of NK4 on hematogenous pulmonary metastasis of the CT26 murine colon cancer cell line, focusing on tumor cell adhesion to endothelial cells. In an in vitro adhesion assay, HGF facilitated adhesion of CT26 cells to a murine endothelial cell line (F-2) in a dose-dependent manner. Furthermore, the enhancing effect of HGF on CT26-F-2 cell interaction was blocked by NK4 as well as by anti-HGF antibody. Similarly, HGF-induced phosphorylation of focal adhesion kinase (FAK), downstream of integrin signaling, was reduced by NK4 and by anti-HGF antibody. However, distinct integrin expression on the surface of CT26 cells was not altered by HGF. In an in vivo experimental pulmonary metastasis assay, stable NK4 expression potently decreased the number of pulmonary metastatic foci. The NK4-induced suppression of pulmonary metastasis was partially reversed when HGF was intraperitoneally administered in an adhesive phase. These results suggest that NK4 could act on tumor cells to inhibit CT26 adhesion to endothelial cells by reducing FAK phosphorylation, which is regulated by inside-out HGF/c-Met signaling, and thereby suppress hematogenous pulmonary metastasis. HGF (dpeaa)DE-He213 c-Met (dpeaa)DE-He213 NK4 (dpeaa)DE-He213 CT26 (dpeaa)DE-He213 Pulmonary metastasis (dpeaa)DE-He213 Endothelial cell (dpeaa)DE-He213 FAK (dpeaa)DE-He213 Taiyoh, Hiroaki verfasserin aut Matsumura, Atsushi verfasserin aut Murayama, Yasutoshi verfasserin aut Ichikawa, Daisuke verfasserin aut Okamoto, Kazuma verfasserin aut Fujiwara, Hitoshi verfasserin aut Ikoma, Hisashi verfasserin aut Nakanishi, Masayoshi verfasserin aut Kikuchi, Shojiro verfasserin aut Sakakura, Chouhei verfasserin aut Ochiai, Toshiya verfasserin aut Kokuba, Yukihito verfasserin aut Taniguchi, Hiroki verfasserin aut Sonoyama, Teruhisa verfasserin aut Matsumoto, Kunio verfasserin aut Nakamura, Toshikazu verfasserin aut Otsuji, Eigo verfasserin aut Enthalten in Clinical & experimental metastasis Dordrecht : Springer Science + Business Media B.V., 1983 26(2009), 5 vom: 21. Feb., Seite 447-456 (DE-627)306354683 (DE-600)1496876-9 1573-7276 nnns volume:26 year:2009 number:5 day:21 month:02 pages:447-456 https://dx.doi.org/10.1007/s10585-009-9244-0 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.81 ASE AR 26 2009 5 21 02 447-456 |
| allfieldsGer |
10.1007/s10585-009-9244-0 doi (DE-627)SPR011488808 (SPR)s10585-009-9244-0-e DE-627 ger DE-627 rakwb eng 610 ASE 44.81 bkl Kubota, Takeshi verfasserin aut NK4, an HGF antagonist, prevents hematogenous pulmonary metastasis by inhibiting adhesion of CT26 cells to endothelial cells 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Hepatocyte growth factor (HGF) plays a definitive role in invasive, angiogenic, and metastatic activities of tumor cells by binding to the c-Met receptor. NK4, a competitive antagonist for HGF and the c-Met receptor, prevents tumor cell growth and metastasis via its bifunctional properties to act as an HGF antagonist and angiogenesis inhibitor. In the present study, we investigated the inhibitory effectiveness of NK4 on hematogenous pulmonary metastasis of the CT26 murine colon cancer cell line, focusing on tumor cell adhesion to endothelial cells. In an in vitro adhesion assay, HGF facilitated adhesion of CT26 cells to a murine endothelial cell line (F-2) in a dose-dependent manner. Furthermore, the enhancing effect of HGF on CT26-F-2 cell interaction was blocked by NK4 as well as by anti-HGF antibody. Similarly, HGF-induced phosphorylation of focal adhesion kinase (FAK), downstream of integrin signaling, was reduced by NK4 and by anti-HGF antibody. However, distinct integrin expression on the surface of CT26 cells was not altered by HGF. In an in vivo experimental pulmonary metastasis assay, stable NK4 expression potently decreased the number of pulmonary metastatic foci. The NK4-induced suppression of pulmonary metastasis was partially reversed when HGF was intraperitoneally administered in an adhesive phase. These results suggest that NK4 could act on tumor cells to inhibit CT26 adhesion to endothelial cells by reducing FAK phosphorylation, which is regulated by inside-out HGF/c-Met signaling, and thereby suppress hematogenous pulmonary metastasis. HGF (dpeaa)DE-He213 c-Met (dpeaa)DE-He213 NK4 (dpeaa)DE-He213 CT26 (dpeaa)DE-He213 Pulmonary metastasis (dpeaa)DE-He213 Endothelial cell (dpeaa)DE-He213 FAK (dpeaa)DE-He213 Taiyoh, Hiroaki verfasserin aut Matsumura, Atsushi verfasserin aut Murayama, Yasutoshi verfasserin aut Ichikawa, Daisuke verfasserin aut Okamoto, Kazuma verfasserin aut Fujiwara, Hitoshi verfasserin aut Ikoma, Hisashi verfasserin aut Nakanishi, Masayoshi verfasserin aut Kikuchi, Shojiro verfasserin aut Sakakura, Chouhei verfasserin aut Ochiai, Toshiya verfasserin aut Kokuba, Yukihito verfasserin aut Taniguchi, Hiroki verfasserin aut Sonoyama, Teruhisa verfasserin aut Matsumoto, Kunio verfasserin aut Nakamura, Toshikazu verfasserin aut Otsuji, Eigo verfasserin aut Enthalten in Clinical & experimental metastasis Dordrecht : Springer Science + Business Media B.V., 1983 26(2009), 5 vom: 21. Feb., Seite 447-456 (DE-627)306354683 (DE-600)1496876-9 1573-7276 nnns volume:26 year:2009 number:5 day:21 month:02 pages:447-456 https://dx.doi.org/10.1007/s10585-009-9244-0 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.81 ASE AR 26 2009 5 21 02 447-456 |
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10.1007/s10585-009-9244-0 doi (DE-627)SPR011488808 (SPR)s10585-009-9244-0-e DE-627 ger DE-627 rakwb eng 610 ASE 44.81 bkl Kubota, Takeshi verfasserin aut NK4, an HGF antagonist, prevents hematogenous pulmonary metastasis by inhibiting adhesion of CT26 cells to endothelial cells 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Hepatocyte growth factor (HGF) plays a definitive role in invasive, angiogenic, and metastatic activities of tumor cells by binding to the c-Met receptor. NK4, a competitive antagonist for HGF and the c-Met receptor, prevents tumor cell growth and metastasis via its bifunctional properties to act as an HGF antagonist and angiogenesis inhibitor. In the present study, we investigated the inhibitory effectiveness of NK4 on hematogenous pulmonary metastasis of the CT26 murine colon cancer cell line, focusing on tumor cell adhesion to endothelial cells. In an in vitro adhesion assay, HGF facilitated adhesion of CT26 cells to a murine endothelial cell line (F-2) in a dose-dependent manner. Furthermore, the enhancing effect of HGF on CT26-F-2 cell interaction was blocked by NK4 as well as by anti-HGF antibody. Similarly, HGF-induced phosphorylation of focal adhesion kinase (FAK), downstream of integrin signaling, was reduced by NK4 and by anti-HGF antibody. However, distinct integrin expression on the surface of CT26 cells was not altered by HGF. In an in vivo experimental pulmonary metastasis assay, stable NK4 expression potently decreased the number of pulmonary metastatic foci. The NK4-induced suppression of pulmonary metastasis was partially reversed when HGF was intraperitoneally administered in an adhesive phase. These results suggest that NK4 could act on tumor cells to inhibit CT26 adhesion to endothelial cells by reducing FAK phosphorylation, which is regulated by inside-out HGF/c-Met signaling, and thereby suppress hematogenous pulmonary metastasis. HGF (dpeaa)DE-He213 c-Met (dpeaa)DE-He213 NK4 (dpeaa)DE-He213 CT26 (dpeaa)DE-He213 Pulmonary metastasis (dpeaa)DE-He213 Endothelial cell (dpeaa)DE-He213 FAK (dpeaa)DE-He213 Taiyoh, Hiroaki verfasserin aut Matsumura, Atsushi verfasserin aut Murayama, Yasutoshi verfasserin aut Ichikawa, Daisuke verfasserin aut Okamoto, Kazuma verfasserin aut Fujiwara, Hitoshi verfasserin aut Ikoma, Hisashi verfasserin aut Nakanishi, Masayoshi verfasserin aut Kikuchi, Shojiro verfasserin aut Sakakura, Chouhei verfasserin aut Ochiai, Toshiya verfasserin aut Kokuba, Yukihito verfasserin aut Taniguchi, Hiroki verfasserin aut Sonoyama, Teruhisa verfasserin aut Matsumoto, Kunio verfasserin aut Nakamura, Toshikazu verfasserin aut Otsuji, Eigo verfasserin aut Enthalten in Clinical & experimental metastasis Dordrecht : Springer Science + Business Media B.V., 1983 26(2009), 5 vom: 21. Feb., Seite 447-456 (DE-627)306354683 (DE-600)1496876-9 1573-7276 nnns volume:26 year:2009 number:5 day:21 month:02 pages:447-456 https://dx.doi.org/10.1007/s10585-009-9244-0 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.81 ASE AR 26 2009 5 21 02 447-456 |
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| source |
Enthalten in Clinical & experimental metastasis 26(2009), 5 vom: 21. Feb., Seite 447-456 volume:26 year:2009 number:5 day:21 month:02 pages:447-456 |
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Enthalten in Clinical & experimental metastasis 26(2009), 5 vom: 21. Feb., Seite 447-456 volume:26 year:2009 number:5 day:21 month:02 pages:447-456 |
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findex.gbv.de |
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HGF c-Met NK4 CT26 Pulmonary metastasis Endothelial cell FAK |
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Kubota, Takeshi @@aut@@ Taiyoh, Hiroaki @@aut@@ Matsumura, Atsushi @@aut@@ Murayama, Yasutoshi @@aut@@ Ichikawa, Daisuke @@aut@@ Okamoto, Kazuma @@aut@@ Fujiwara, Hitoshi @@aut@@ Ikoma, Hisashi @@aut@@ Nakanishi, Masayoshi @@aut@@ Kikuchi, Shojiro @@aut@@ Sakakura, Chouhei @@aut@@ Ochiai, Toshiya @@aut@@ Kokuba, Yukihito @@aut@@ Taniguchi, Hiroki @@aut@@ Sonoyama, Teruhisa @@aut@@ Matsumoto, Kunio @@aut@@ Nakamura, Toshikazu @@aut@@ Otsuji, Eigo @@aut@@ |
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2009-02-21T00:00:00Z |
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3610 |
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englisch |
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| author |
Kubota, Takeshi |
| spellingShingle |
Kubota, Takeshi ddc 610 bkl 44.81 misc HGF misc c-Met misc NK4 misc CT26 misc Pulmonary metastasis misc Endothelial cell misc FAK NK4, an HGF antagonist, prevents hematogenous pulmonary metastasis by inhibiting adhesion of CT26 cells to endothelial cells |
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610 ASE 44.81 bkl NK4, an HGF antagonist, prevents hematogenous pulmonary metastasis by inhibiting adhesion of CT26 cells to endothelial cells HGF (dpeaa)DE-He213 c-Met (dpeaa)DE-He213 NK4 (dpeaa)DE-He213 CT26 (dpeaa)DE-He213 Pulmonary metastasis (dpeaa)DE-He213 Endothelial cell (dpeaa)DE-He213 FAK (dpeaa)DE-He213 |
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ddc 610 bkl 44.81 misc HGF misc c-Met misc NK4 misc CT26 misc Pulmonary metastasis misc Endothelial cell misc FAK |
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ddc 610 bkl 44.81 misc HGF misc c-Met misc NK4 misc CT26 misc Pulmonary metastasis misc Endothelial cell misc FAK |
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ddc 610 bkl 44.81 misc HGF misc c-Met misc NK4 misc CT26 misc Pulmonary metastasis misc Endothelial cell misc FAK |
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NK4, an HGF antagonist, prevents hematogenous pulmonary metastasis by inhibiting adhesion of CT26 cells to endothelial cells |
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NK4, an HGF antagonist, prevents hematogenous pulmonary metastasis by inhibiting adhesion of CT26 cells to endothelial cells |
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Kubota, Takeshi |
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Kubota, Takeshi Taiyoh, Hiroaki Matsumura, Atsushi Murayama, Yasutoshi Ichikawa, Daisuke Okamoto, Kazuma Fujiwara, Hitoshi Ikoma, Hisashi Nakanishi, Masayoshi Kikuchi, Shojiro Sakakura, Chouhei Ochiai, Toshiya Kokuba, Yukihito Taniguchi, Hiroki Sonoyama, Teruhisa Matsumoto, Kunio Nakamura, Toshikazu Otsuji, Eigo |
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10.1007/s10585-009-9244-0 |
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610 |
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verfasserin |
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nk4, an hgf antagonist, prevents hematogenous pulmonary metastasis by inhibiting adhesion of ct26 cells to endothelial cells |
| title_auth |
NK4, an HGF antagonist, prevents hematogenous pulmonary metastasis by inhibiting adhesion of CT26 cells to endothelial cells |
| abstract |
Abstract Hepatocyte growth factor (HGF) plays a definitive role in invasive, angiogenic, and metastatic activities of tumor cells by binding to the c-Met receptor. NK4, a competitive antagonist for HGF and the c-Met receptor, prevents tumor cell growth and metastasis via its bifunctional properties to act as an HGF antagonist and angiogenesis inhibitor. In the present study, we investigated the inhibitory effectiveness of NK4 on hematogenous pulmonary metastasis of the CT26 murine colon cancer cell line, focusing on tumor cell adhesion to endothelial cells. In an in vitro adhesion assay, HGF facilitated adhesion of CT26 cells to a murine endothelial cell line (F-2) in a dose-dependent manner. Furthermore, the enhancing effect of HGF on CT26-F-2 cell interaction was blocked by NK4 as well as by anti-HGF antibody. Similarly, HGF-induced phosphorylation of focal adhesion kinase (FAK), downstream of integrin signaling, was reduced by NK4 and by anti-HGF antibody. However, distinct integrin expression on the surface of CT26 cells was not altered by HGF. In an in vivo experimental pulmonary metastasis assay, stable NK4 expression potently decreased the number of pulmonary metastatic foci. The NK4-induced suppression of pulmonary metastasis was partially reversed when HGF was intraperitoneally administered in an adhesive phase. These results suggest that NK4 could act on tumor cells to inhibit CT26 adhesion to endothelial cells by reducing FAK phosphorylation, which is regulated by inside-out HGF/c-Met signaling, and thereby suppress hematogenous pulmonary metastasis. |
| abstractGer |
Abstract Hepatocyte growth factor (HGF) plays a definitive role in invasive, angiogenic, and metastatic activities of tumor cells by binding to the c-Met receptor. NK4, a competitive antagonist for HGF and the c-Met receptor, prevents tumor cell growth and metastasis via its bifunctional properties to act as an HGF antagonist and angiogenesis inhibitor. In the present study, we investigated the inhibitory effectiveness of NK4 on hematogenous pulmonary metastasis of the CT26 murine colon cancer cell line, focusing on tumor cell adhesion to endothelial cells. In an in vitro adhesion assay, HGF facilitated adhesion of CT26 cells to a murine endothelial cell line (F-2) in a dose-dependent manner. Furthermore, the enhancing effect of HGF on CT26-F-2 cell interaction was blocked by NK4 as well as by anti-HGF antibody. Similarly, HGF-induced phosphorylation of focal adhesion kinase (FAK), downstream of integrin signaling, was reduced by NK4 and by anti-HGF antibody. However, distinct integrin expression on the surface of CT26 cells was not altered by HGF. In an in vivo experimental pulmonary metastasis assay, stable NK4 expression potently decreased the number of pulmonary metastatic foci. The NK4-induced suppression of pulmonary metastasis was partially reversed when HGF was intraperitoneally administered in an adhesive phase. These results suggest that NK4 could act on tumor cells to inhibit CT26 adhesion to endothelial cells by reducing FAK phosphorylation, which is regulated by inside-out HGF/c-Met signaling, and thereby suppress hematogenous pulmonary metastasis. |
| abstract_unstemmed |
Abstract Hepatocyte growth factor (HGF) plays a definitive role in invasive, angiogenic, and metastatic activities of tumor cells by binding to the c-Met receptor. NK4, a competitive antagonist for HGF and the c-Met receptor, prevents tumor cell growth and metastasis via its bifunctional properties to act as an HGF antagonist and angiogenesis inhibitor. In the present study, we investigated the inhibitory effectiveness of NK4 on hematogenous pulmonary metastasis of the CT26 murine colon cancer cell line, focusing on tumor cell adhesion to endothelial cells. In an in vitro adhesion assay, HGF facilitated adhesion of CT26 cells to a murine endothelial cell line (F-2) in a dose-dependent manner. Furthermore, the enhancing effect of HGF on CT26-F-2 cell interaction was blocked by NK4 as well as by anti-HGF antibody. Similarly, HGF-induced phosphorylation of focal adhesion kinase (FAK), downstream of integrin signaling, was reduced by NK4 and by anti-HGF antibody. However, distinct integrin expression on the surface of CT26 cells was not altered by HGF. In an in vivo experimental pulmonary metastasis assay, stable NK4 expression potently decreased the number of pulmonary metastatic foci. The NK4-induced suppression of pulmonary metastasis was partially reversed when HGF was intraperitoneally administered in an adhesive phase. These results suggest that NK4 could act on tumor cells to inhibit CT26 adhesion to endothelial cells by reducing FAK phosphorylation, which is regulated by inside-out HGF/c-Met signaling, and thereby suppress hematogenous pulmonary metastasis. |
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NK4, an HGF antagonist, prevents hematogenous pulmonary metastasis by inhibiting adhesion of CT26 cells to endothelial cells |
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https://dx.doi.org/10.1007/s10585-009-9244-0 |
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Taiyoh, Hiroaki Matsumura, Atsushi Murayama, Yasutoshi Ichikawa, Daisuke Okamoto, Kazuma Fujiwara, Hitoshi Ikoma, Hisashi Nakanishi, Masayoshi Kikuchi, Shojiro Sakakura, Chouhei Ochiai, Toshiya Kokuba, Yukihito Taniguchi, Hiroki Sonoyama, Teruhisa Matsumoto, Kunio Nakamura, Toshikazu Otsuji, Eigo |
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Taiyoh, Hiroaki Matsumura, Atsushi Murayama, Yasutoshi Ichikawa, Daisuke Okamoto, Kazuma Fujiwara, Hitoshi Ikoma, Hisashi Nakanishi, Masayoshi Kikuchi, Shojiro Sakakura, Chouhei Ochiai, Toshiya Kokuba, Yukihito Taniguchi, Hiroki Sonoyama, Teruhisa Matsumoto, Kunio Nakamura, Toshikazu Otsuji, Eigo |
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10.1007/s10585-009-9244-0 |
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2024-07-03T22:57:30.797Z |
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| score |
7.3997955 |