Role of L1 cell adhesion molecule (L1CAM) in the metastatic cascade: promotion of dissemination, colonization, and metastatic growth
Abstract Expression of the L1 cell adhesion molecule (L1CAM) is frequently increased in cancer patients compared to healthy individuals and also linked with bad prognosis of solid tumours. Previously, we could show that full-length L1CAM promotes metastasis formation via up-regulation of gelatinolyt...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Weinspach, Dirk [verfasserIn] Seubert, Bastian [verfasserIn] Schaten, Susanne [verfasserIn] Honert, Katja [verfasserIn] Sebens, Susanne [verfasserIn] Altevogt, Peter [verfasserIn] Krüger, Achim [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2013 |
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| Schlagwörter: |
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| Übergeordnetes Werk: |
Enthalten in: Clinical & experimental metastasis - Dordrecht : Springer Science + Business Media B.V., 1983, 31(2013), 1 vom: 04. Sept., Seite 87-100 |
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| Übergeordnetes Werk: |
volume:31 ; year:2013 ; number:1 ; day:04 ; month:09 ; pages:87-100 |
| Links: |
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| DOI / URN: |
10.1007/s10585-013-9613-6 |
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| Katalog-ID: |
SPR011492864 |
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| 520 | |a Abstract Expression of the L1 cell adhesion molecule (L1CAM) is frequently increased in cancer patients compared to healthy individuals and also linked with bad prognosis of solid tumours. Previously, we could show that full-length L1CAM promotes metastasis formation via up-regulation of gelatinolytic activity in fibrosarcoma. In this study, we aimed to extend this finding to haematogenous malignancies and carcinomas, and to specifically elucidate the impact of L1CAM on major steps of the metastatic cascade. In a well-established T-cell lymphoma spontaneous metastasis model, silencing of L1CAM significantly improved survival of the mice, while intradermal tumour growth remained unaltered. This correlated with significantly decreased spontaneous metastasis formation. L1CAM suppression abrogated the metastatic potential of T-cell lymphoma as well as carcinoma cells as demonstrated by reduced migration and invasion in vitro and reduced formation of experimental metastasis in vivo. At the molecular level, silencing of L1CAM led to reduced expression of gelatinases MMP-2 and -9 in vitro and decreased gelatinolytic activity in primary tumours and metastases in vivo. In accordance, knock down of L1CAM had similar suppressive effects on migration, invasion and in vivo-gelatinolytic activity as treatment with the specific gelatinase inhibitor SB-3CT. This newly discovered impact of L1CAM on distinct steps of the metastatic cascade and MMP activity highlights the potential of possible L1CAM-directed therapies to inhibit metastatic spread. | ||
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| 650 | 4 | |a Metastatic cascade |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Dissemination |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Metastatic growth |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a MMPs |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Targeted therapy |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Seubert, Bastian |e verfasserin |4 aut | |
| 700 | 1 | |a Schaten, Susanne |e verfasserin |4 aut | |
| 700 | 1 | |a Honert, Katja |e verfasserin |4 aut | |
| 700 | 1 | |a Sebens, Susanne |e verfasserin |4 aut | |
| 700 | 1 | |a Altevogt, Peter |e verfasserin |4 aut | |
| 700 | 1 | |a Krüger, Achim |e verfasserin |4 aut | |
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10.1007/s10585-013-9613-6 doi (DE-627)SPR011492864 (SPR)s10585-013-9613-6-e DE-627 ger DE-627 rakwb eng 610 ASE 44.81 bkl Weinspach, Dirk verfasserin aut Role of L1 cell adhesion molecule (L1CAM) in the metastatic cascade: promotion of dissemination, colonization, and metastatic growth 2013 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Expression of the L1 cell adhesion molecule (L1CAM) is frequently increased in cancer patients compared to healthy individuals and also linked with bad prognosis of solid tumours. Previously, we could show that full-length L1CAM promotes metastasis formation via up-regulation of gelatinolytic activity in fibrosarcoma. In this study, we aimed to extend this finding to haematogenous malignancies and carcinomas, and to specifically elucidate the impact of L1CAM on major steps of the metastatic cascade. In a well-established T-cell lymphoma spontaneous metastasis model, silencing of L1CAM significantly improved survival of the mice, while intradermal tumour growth remained unaltered. This correlated with significantly decreased spontaneous metastasis formation. L1CAM suppression abrogated the metastatic potential of T-cell lymphoma as well as carcinoma cells as demonstrated by reduced migration and invasion in vitro and reduced formation of experimental metastasis in vivo. At the molecular level, silencing of L1CAM led to reduced expression of gelatinases MMP-2 and -9 in vitro and decreased gelatinolytic activity in primary tumours and metastases in vivo. In accordance, knock down of L1CAM had similar suppressive effects on migration, invasion and in vivo-gelatinolytic activity as treatment with the specific gelatinase inhibitor SB-3CT. This newly discovered impact of L1CAM on distinct steps of the metastatic cascade and MMP activity highlights the potential of possible L1CAM-directed therapies to inhibit metastatic spread. L1CAM (dpeaa)DE-He213 Metastatic cascade (dpeaa)DE-He213 Dissemination (dpeaa)DE-He213 Metastatic growth (dpeaa)DE-He213 MMPs (dpeaa)DE-He213 Targeted therapy (dpeaa)DE-He213 Seubert, Bastian verfasserin aut Schaten, Susanne verfasserin aut Honert, Katja verfasserin aut Sebens, Susanne verfasserin aut Altevogt, Peter verfasserin aut Krüger, Achim verfasserin aut Enthalten in Clinical & experimental metastasis Dordrecht : Springer Science + Business Media B.V., 1983 31(2013), 1 vom: 04. Sept., Seite 87-100 (DE-627)306354683 (DE-600)1496876-9 1573-7276 nnns volume:31 year:2013 number:1 day:04 month:09 pages:87-100 https://dx.doi.org/10.1007/s10585-013-9613-6 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 31 2013 1 04 09 87-100 |
| spelling |
10.1007/s10585-013-9613-6 doi (DE-627)SPR011492864 (SPR)s10585-013-9613-6-e DE-627 ger DE-627 rakwb eng 610 ASE 44.81 bkl Weinspach, Dirk verfasserin aut Role of L1 cell adhesion molecule (L1CAM) in the metastatic cascade: promotion of dissemination, colonization, and metastatic growth 2013 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Expression of the L1 cell adhesion molecule (L1CAM) is frequently increased in cancer patients compared to healthy individuals and also linked with bad prognosis of solid tumours. Previously, we could show that full-length L1CAM promotes metastasis formation via up-regulation of gelatinolytic activity in fibrosarcoma. In this study, we aimed to extend this finding to haematogenous malignancies and carcinomas, and to specifically elucidate the impact of L1CAM on major steps of the metastatic cascade. In a well-established T-cell lymphoma spontaneous metastasis model, silencing of L1CAM significantly improved survival of the mice, while intradermal tumour growth remained unaltered. This correlated with significantly decreased spontaneous metastasis formation. L1CAM suppression abrogated the metastatic potential of T-cell lymphoma as well as carcinoma cells as demonstrated by reduced migration and invasion in vitro and reduced formation of experimental metastasis in vivo. At the molecular level, silencing of L1CAM led to reduced expression of gelatinases MMP-2 and -9 in vitro and decreased gelatinolytic activity in primary tumours and metastases in vivo. In accordance, knock down of L1CAM had similar suppressive effects on migration, invasion and in vivo-gelatinolytic activity as treatment with the specific gelatinase inhibitor SB-3CT. This newly discovered impact of L1CAM on distinct steps of the metastatic cascade and MMP activity highlights the potential of possible L1CAM-directed therapies to inhibit metastatic spread. L1CAM (dpeaa)DE-He213 Metastatic cascade (dpeaa)DE-He213 Dissemination (dpeaa)DE-He213 Metastatic growth (dpeaa)DE-He213 MMPs (dpeaa)DE-He213 Targeted therapy (dpeaa)DE-He213 Seubert, Bastian verfasserin aut Schaten, Susanne verfasserin aut Honert, Katja verfasserin aut Sebens, Susanne verfasserin aut Altevogt, Peter verfasserin aut Krüger, Achim verfasserin aut Enthalten in Clinical & experimental metastasis Dordrecht : Springer Science + Business Media B.V., 1983 31(2013), 1 vom: 04. Sept., Seite 87-100 (DE-627)306354683 (DE-600)1496876-9 1573-7276 nnns volume:31 year:2013 number:1 day:04 month:09 pages:87-100 https://dx.doi.org/10.1007/s10585-013-9613-6 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 31 2013 1 04 09 87-100 |
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10.1007/s10585-013-9613-6 doi (DE-627)SPR011492864 (SPR)s10585-013-9613-6-e DE-627 ger DE-627 rakwb eng 610 ASE 44.81 bkl Weinspach, Dirk verfasserin aut Role of L1 cell adhesion molecule (L1CAM) in the metastatic cascade: promotion of dissemination, colonization, and metastatic growth 2013 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Expression of the L1 cell adhesion molecule (L1CAM) is frequently increased in cancer patients compared to healthy individuals and also linked with bad prognosis of solid tumours. Previously, we could show that full-length L1CAM promotes metastasis formation via up-regulation of gelatinolytic activity in fibrosarcoma. In this study, we aimed to extend this finding to haematogenous malignancies and carcinomas, and to specifically elucidate the impact of L1CAM on major steps of the metastatic cascade. In a well-established T-cell lymphoma spontaneous metastasis model, silencing of L1CAM significantly improved survival of the mice, while intradermal tumour growth remained unaltered. This correlated with significantly decreased spontaneous metastasis formation. L1CAM suppression abrogated the metastatic potential of T-cell lymphoma as well as carcinoma cells as demonstrated by reduced migration and invasion in vitro and reduced formation of experimental metastasis in vivo. At the molecular level, silencing of L1CAM led to reduced expression of gelatinases MMP-2 and -9 in vitro and decreased gelatinolytic activity in primary tumours and metastases in vivo. In accordance, knock down of L1CAM had similar suppressive effects on migration, invasion and in vivo-gelatinolytic activity as treatment with the specific gelatinase inhibitor SB-3CT. This newly discovered impact of L1CAM on distinct steps of the metastatic cascade and MMP activity highlights the potential of possible L1CAM-directed therapies to inhibit metastatic spread. L1CAM (dpeaa)DE-He213 Metastatic cascade (dpeaa)DE-He213 Dissemination (dpeaa)DE-He213 Metastatic growth (dpeaa)DE-He213 MMPs (dpeaa)DE-He213 Targeted therapy (dpeaa)DE-He213 Seubert, Bastian verfasserin aut Schaten, Susanne verfasserin aut Honert, Katja verfasserin aut Sebens, Susanne verfasserin aut Altevogt, Peter verfasserin aut Krüger, Achim verfasserin aut Enthalten in Clinical & experimental metastasis Dordrecht : Springer Science + Business Media B.V., 1983 31(2013), 1 vom: 04. Sept., Seite 87-100 (DE-627)306354683 (DE-600)1496876-9 1573-7276 nnns volume:31 year:2013 number:1 day:04 month:09 pages:87-100 https://dx.doi.org/10.1007/s10585-013-9613-6 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 31 2013 1 04 09 87-100 |
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10.1007/s10585-013-9613-6 doi (DE-627)SPR011492864 (SPR)s10585-013-9613-6-e DE-627 ger DE-627 rakwb eng 610 ASE 44.81 bkl Weinspach, Dirk verfasserin aut Role of L1 cell adhesion molecule (L1CAM) in the metastatic cascade: promotion of dissemination, colonization, and metastatic growth 2013 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Expression of the L1 cell adhesion molecule (L1CAM) is frequently increased in cancer patients compared to healthy individuals and also linked with bad prognosis of solid tumours. Previously, we could show that full-length L1CAM promotes metastasis formation via up-regulation of gelatinolytic activity in fibrosarcoma. In this study, we aimed to extend this finding to haematogenous malignancies and carcinomas, and to specifically elucidate the impact of L1CAM on major steps of the metastatic cascade. In a well-established T-cell lymphoma spontaneous metastasis model, silencing of L1CAM significantly improved survival of the mice, while intradermal tumour growth remained unaltered. This correlated with significantly decreased spontaneous metastasis formation. L1CAM suppression abrogated the metastatic potential of T-cell lymphoma as well as carcinoma cells as demonstrated by reduced migration and invasion in vitro and reduced formation of experimental metastasis in vivo. At the molecular level, silencing of L1CAM led to reduced expression of gelatinases MMP-2 and -9 in vitro and decreased gelatinolytic activity in primary tumours and metastases in vivo. In accordance, knock down of L1CAM had similar suppressive effects on migration, invasion and in vivo-gelatinolytic activity as treatment with the specific gelatinase inhibitor SB-3CT. This newly discovered impact of L1CAM on distinct steps of the metastatic cascade and MMP activity highlights the potential of possible L1CAM-directed therapies to inhibit metastatic spread. L1CAM (dpeaa)DE-He213 Metastatic cascade (dpeaa)DE-He213 Dissemination (dpeaa)DE-He213 Metastatic growth (dpeaa)DE-He213 MMPs (dpeaa)DE-He213 Targeted therapy (dpeaa)DE-He213 Seubert, Bastian verfasserin aut Schaten, Susanne verfasserin aut Honert, Katja verfasserin aut Sebens, Susanne verfasserin aut Altevogt, Peter verfasserin aut Krüger, Achim verfasserin aut Enthalten in Clinical & experimental metastasis Dordrecht : Springer Science + Business Media B.V., 1983 31(2013), 1 vom: 04. Sept., Seite 87-100 (DE-627)306354683 (DE-600)1496876-9 1573-7276 nnns volume:31 year:2013 number:1 day:04 month:09 pages:87-100 https://dx.doi.org/10.1007/s10585-013-9613-6 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 31 2013 1 04 09 87-100 |
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10.1007/s10585-013-9613-6 doi (DE-627)SPR011492864 (SPR)s10585-013-9613-6-e DE-627 ger DE-627 rakwb eng 610 ASE 44.81 bkl Weinspach, Dirk verfasserin aut Role of L1 cell adhesion molecule (L1CAM) in the metastatic cascade: promotion of dissemination, colonization, and metastatic growth 2013 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Expression of the L1 cell adhesion molecule (L1CAM) is frequently increased in cancer patients compared to healthy individuals and also linked with bad prognosis of solid tumours. Previously, we could show that full-length L1CAM promotes metastasis formation via up-regulation of gelatinolytic activity in fibrosarcoma. In this study, we aimed to extend this finding to haematogenous malignancies and carcinomas, and to specifically elucidate the impact of L1CAM on major steps of the metastatic cascade. In a well-established T-cell lymphoma spontaneous metastasis model, silencing of L1CAM significantly improved survival of the mice, while intradermal tumour growth remained unaltered. This correlated with significantly decreased spontaneous metastasis formation. L1CAM suppression abrogated the metastatic potential of T-cell lymphoma as well as carcinoma cells as demonstrated by reduced migration and invasion in vitro and reduced formation of experimental metastasis in vivo. At the molecular level, silencing of L1CAM led to reduced expression of gelatinases MMP-2 and -9 in vitro and decreased gelatinolytic activity in primary tumours and metastases in vivo. In accordance, knock down of L1CAM had similar suppressive effects on migration, invasion and in vivo-gelatinolytic activity as treatment with the specific gelatinase inhibitor SB-3CT. This newly discovered impact of L1CAM on distinct steps of the metastatic cascade and MMP activity highlights the potential of possible L1CAM-directed therapies to inhibit metastatic spread. L1CAM (dpeaa)DE-He213 Metastatic cascade (dpeaa)DE-He213 Dissemination (dpeaa)DE-He213 Metastatic growth (dpeaa)DE-He213 MMPs (dpeaa)DE-He213 Targeted therapy (dpeaa)DE-He213 Seubert, Bastian verfasserin aut Schaten, Susanne verfasserin aut Honert, Katja verfasserin aut Sebens, Susanne verfasserin aut Altevogt, Peter verfasserin aut Krüger, Achim verfasserin aut Enthalten in Clinical & experimental metastasis Dordrecht : Springer Science + Business Media B.V., 1983 31(2013), 1 vom: 04. Sept., Seite 87-100 (DE-627)306354683 (DE-600)1496876-9 1573-7276 nnns volume:31 year:2013 number:1 day:04 month:09 pages:87-100 https://dx.doi.org/10.1007/s10585-013-9613-6 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 31 2013 1 04 09 87-100 |
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Enthalten in Clinical & experimental metastasis 31(2013), 1 vom: 04. Sept., Seite 87-100 volume:31 year:2013 number:1 day:04 month:09 pages:87-100 |
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Enthalten in Clinical & experimental metastasis 31(2013), 1 vom: 04. Sept., Seite 87-100 volume:31 year:2013 number:1 day:04 month:09 pages:87-100 |
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L1CAM Metastatic cascade Dissemination Metastatic growth MMPs Targeted therapy |
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Clinical & experimental metastasis |
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Weinspach, Dirk @@aut@@ Seubert, Bastian @@aut@@ Schaten, Susanne @@aut@@ Honert, Katja @@aut@@ Sebens, Susanne @@aut@@ Altevogt, Peter @@aut@@ Krüger, Achim @@aut@@ |
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Previously, we could show that full-length L1CAM promotes metastasis formation via up-regulation of gelatinolytic activity in fibrosarcoma. In this study, we aimed to extend this finding to haematogenous malignancies and carcinomas, and to specifically elucidate the impact of L1CAM on major steps of the metastatic cascade. In a well-established T-cell lymphoma spontaneous metastasis model, silencing of L1CAM significantly improved survival of the mice, while intradermal tumour growth remained unaltered. This correlated with significantly decreased spontaneous metastasis formation. L1CAM suppression abrogated the metastatic potential of T-cell lymphoma as well as carcinoma cells as demonstrated by reduced migration and invasion in vitro and reduced formation of experimental metastasis in vivo. At the molecular level, silencing of L1CAM led to reduced expression of gelatinases MMP-2 and -9 in vitro and decreased gelatinolytic activity in primary tumours and metastases in vivo. In accordance, knock down of L1CAM had similar suppressive effects on migration, invasion and in vivo-gelatinolytic activity as treatment with the specific gelatinase inhibitor SB-3CT. 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Weinspach, Dirk |
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Weinspach, Dirk ddc 610 bkl 44.81 misc L1CAM misc Metastatic cascade misc Dissemination misc Metastatic growth misc MMPs misc Targeted therapy Role of L1 cell adhesion molecule (L1CAM) in the metastatic cascade: promotion of dissemination, colonization, and metastatic growth |
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610 ASE 44.81 bkl Role of L1 cell adhesion molecule (L1CAM) in the metastatic cascade: promotion of dissemination, colonization, and metastatic growth L1CAM (dpeaa)DE-He213 Metastatic cascade (dpeaa)DE-He213 Dissemination (dpeaa)DE-He213 Metastatic growth (dpeaa)DE-He213 MMPs (dpeaa)DE-He213 Targeted therapy (dpeaa)DE-He213 |
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Weinspach, Dirk |
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role of l1 cell adhesion molecule (l1cam) in the metastatic cascade: promotion of dissemination, colonization, and metastatic growth |
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Role of L1 cell adhesion molecule (L1CAM) in the metastatic cascade: promotion of dissemination, colonization, and metastatic growth |
| abstract |
Abstract Expression of the L1 cell adhesion molecule (L1CAM) is frequently increased in cancer patients compared to healthy individuals and also linked with bad prognosis of solid tumours. Previously, we could show that full-length L1CAM promotes metastasis formation via up-regulation of gelatinolytic activity in fibrosarcoma. In this study, we aimed to extend this finding to haematogenous malignancies and carcinomas, and to specifically elucidate the impact of L1CAM on major steps of the metastatic cascade. In a well-established T-cell lymphoma spontaneous metastasis model, silencing of L1CAM significantly improved survival of the mice, while intradermal tumour growth remained unaltered. This correlated with significantly decreased spontaneous metastasis formation. L1CAM suppression abrogated the metastatic potential of T-cell lymphoma as well as carcinoma cells as demonstrated by reduced migration and invasion in vitro and reduced formation of experimental metastasis in vivo. At the molecular level, silencing of L1CAM led to reduced expression of gelatinases MMP-2 and -9 in vitro and decreased gelatinolytic activity in primary tumours and metastases in vivo. In accordance, knock down of L1CAM had similar suppressive effects on migration, invasion and in vivo-gelatinolytic activity as treatment with the specific gelatinase inhibitor SB-3CT. This newly discovered impact of L1CAM on distinct steps of the metastatic cascade and MMP activity highlights the potential of possible L1CAM-directed therapies to inhibit metastatic spread. |
| abstractGer |
Abstract Expression of the L1 cell adhesion molecule (L1CAM) is frequently increased in cancer patients compared to healthy individuals and also linked with bad prognosis of solid tumours. Previously, we could show that full-length L1CAM promotes metastasis formation via up-regulation of gelatinolytic activity in fibrosarcoma. In this study, we aimed to extend this finding to haematogenous malignancies and carcinomas, and to specifically elucidate the impact of L1CAM on major steps of the metastatic cascade. In a well-established T-cell lymphoma spontaneous metastasis model, silencing of L1CAM significantly improved survival of the mice, while intradermal tumour growth remained unaltered. This correlated with significantly decreased spontaneous metastasis formation. L1CAM suppression abrogated the metastatic potential of T-cell lymphoma as well as carcinoma cells as demonstrated by reduced migration and invasion in vitro and reduced formation of experimental metastasis in vivo. At the molecular level, silencing of L1CAM led to reduced expression of gelatinases MMP-2 and -9 in vitro and decreased gelatinolytic activity in primary tumours and metastases in vivo. In accordance, knock down of L1CAM had similar suppressive effects on migration, invasion and in vivo-gelatinolytic activity as treatment with the specific gelatinase inhibitor SB-3CT. This newly discovered impact of L1CAM on distinct steps of the metastatic cascade and MMP activity highlights the potential of possible L1CAM-directed therapies to inhibit metastatic spread. |
| abstract_unstemmed |
Abstract Expression of the L1 cell adhesion molecule (L1CAM) is frequently increased in cancer patients compared to healthy individuals and also linked with bad prognosis of solid tumours. Previously, we could show that full-length L1CAM promotes metastasis formation via up-regulation of gelatinolytic activity in fibrosarcoma. In this study, we aimed to extend this finding to haematogenous malignancies and carcinomas, and to specifically elucidate the impact of L1CAM on major steps of the metastatic cascade. In a well-established T-cell lymphoma spontaneous metastasis model, silencing of L1CAM significantly improved survival of the mice, while intradermal tumour growth remained unaltered. This correlated with significantly decreased spontaneous metastasis formation. L1CAM suppression abrogated the metastatic potential of T-cell lymphoma as well as carcinoma cells as demonstrated by reduced migration and invasion in vitro and reduced formation of experimental metastasis in vivo. At the molecular level, silencing of L1CAM led to reduced expression of gelatinases MMP-2 and -9 in vitro and decreased gelatinolytic activity in primary tumours and metastases in vivo. In accordance, knock down of L1CAM had similar suppressive effects on migration, invasion and in vivo-gelatinolytic activity as treatment with the specific gelatinase inhibitor SB-3CT. This newly discovered impact of L1CAM on distinct steps of the metastatic cascade and MMP activity highlights the potential of possible L1CAM-directed therapies to inhibit metastatic spread. |
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Role of L1 cell adhesion molecule (L1CAM) in the metastatic cascade: promotion of dissemination, colonization, and metastatic growth |
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Seubert, Bastian Schaten, Susanne Honert, Katja Sebens, Susanne Altevogt, Peter Krüger, Achim |
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| score |
7.397958 |