Src activation of Stat3 is an independent requirement from NF-κB activation for constitutive IL-8 expression in human pancreatic adenocarcinoma cells
Abstract Human pancreatic tumors often overexpress the angiogenesis-promoting factor Interleukin 8 (IL-8), in part due to overexpression of NF-κB, a frequent occurrence in pancreatic adenocarcinoma. In this study, we demonstrate that reducing c-Src kinase activity, through either pharmacologic inhib...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Trevino, Jose G. [verfasserIn] Gray, Michael J. [verfasserIn] Nawrocki, Steffan T. [verfasserIn] Summy, Justin M. [verfasserIn] Lesslie, Donald P. [verfasserIn] Evans, Douglas B. [verfasserIn] Sawyer, Tomi K. [verfasserIn] Shakespeare, William C. [verfasserIn] Watowich, Stephanie S. [verfasserIn] Chiao, Paul J. [verfasserIn] McConkey, David J. [verfasserIn] Gallick, Gary E. [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2006 |
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| Schlagwörter: |
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| Übergeordnetes Werk: |
Enthalten in: Angiogenesis - Dordrecht [u.a.] : Springer Science + Business Media B.V, 1997, 9(2006), 2 vom: Juni, Seite 101-110 |
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| Übergeordnetes Werk: |
volume:9 ; year:2006 ; number:2 ; month:06 ; pages:101-110 |
| Links: |
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| DOI / URN: |
10.1007/s10456-006-9038-9 |
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| Katalog-ID: |
SPR010159835 |
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| 100 | 1 | |a Trevino, Jose G. |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Src activation of Stat3 is an independent requirement from NF-κB activation for constitutive IL-8 expression in human pancreatic adenocarcinoma cells |
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| 520 | |a Abstract Human pancreatic tumors often overexpress the angiogenesis-promoting factor Interleukin 8 (IL-8), in part due to overexpression of NF-κB, a frequent occurrence in pancreatic adenocarcinoma. In this study, we demonstrate that reducing c-Src kinase activity, through either pharmacologic inhibition or small interfering RNA-targeted reduction of Src expression, significantly decreased IL-8 expression (P < 0.05) without affecting NF-κB-mediated transcription, but by decreasing phosphorylation of STAT3. To ascertain whether Src-mediated expression of IL-8 was dependent on STAT3, we used stable clones expressing a dominant-negative isoform of STAT3 that inhibits endogenous STAT3 phosphorylation and subsequent DNA binding and STAT3-mediated gene expression or a constitutively activated isoform of STAT3. IL-8 expression was significantly lower in clones expressing the dominant-negative isoform and significantly increased in clones expressing the activated isoform (P < 0.05 for both). Pharmacologic inhibition of NF-κB activity significantly reduced basal IL-8 expression and tumor necrosis factor-induced IL-8 expression (P < 0.05 for both), yet NF-κB activity was not dependent on Src. We therefore suggest that Src activation, through phosphorylation of␣STAT3, and NF-κB are all required for expression of IL-8 a critical angiogenic-promoting factor in pancreatic adenocarcinomas. | ||
| 650 | 4 | |a Angiogenesis |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a IL-8 |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Src |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a NF-κB |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a STAT3 |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a NF-kappaB |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Pancreatic adenocarcinoma |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Gray, Michael J. |e verfasserin |4 aut | |
| 700 | 1 | |a Nawrocki, Steffan T. |e verfasserin |4 aut | |
| 700 | 1 | |a Summy, Justin M. |e verfasserin |4 aut | |
| 700 | 1 | |a Lesslie, Donald P. |e verfasserin |4 aut | |
| 700 | 1 | |a Evans, Douglas B. |e verfasserin |4 aut | |
| 700 | 1 | |a Sawyer, Tomi K. |e verfasserin |4 aut | |
| 700 | 1 | |a Shakespeare, William C. |e verfasserin |4 aut | |
| 700 | 1 | |a Watowich, Stephanie S. |e verfasserin |4 aut | |
| 700 | 1 | |a Chiao, Paul J. |e verfasserin |4 aut | |
| 700 | 1 | |a McConkey, David J. |e verfasserin |4 aut | |
| 700 | 1 | |a Gallick, Gary E. |e verfasserin |4 aut | |
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10.1007/s10456-006-9038-9 doi (DE-627)SPR010159835 (SPR)s10456-006-9038-9-e DE-627 ger DE-627 rakwb eng 610 ASE 44.85 bkl Trevino, Jose G. verfasserin aut Src activation of Stat3 is an independent requirement from NF-κB activation for constitutive IL-8 expression in human pancreatic adenocarcinoma cells 2006 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Human pancreatic tumors often overexpress the angiogenesis-promoting factor Interleukin 8 (IL-8), in part due to overexpression of NF-κB, a frequent occurrence in pancreatic adenocarcinoma. In this study, we demonstrate that reducing c-Src kinase activity, through either pharmacologic inhibition or small interfering RNA-targeted reduction of Src expression, significantly decreased IL-8 expression (P < 0.05) without affecting NF-κB-mediated transcription, but by decreasing phosphorylation of STAT3. To ascertain whether Src-mediated expression of IL-8 was dependent on STAT3, we used stable clones expressing a dominant-negative isoform of STAT3 that inhibits endogenous STAT3 phosphorylation and subsequent DNA binding and STAT3-mediated gene expression or a constitutively activated isoform of STAT3. IL-8 expression was significantly lower in clones expressing the dominant-negative isoform and significantly increased in clones expressing the activated isoform (P < 0.05 for both). Pharmacologic inhibition of NF-κB activity significantly reduced basal IL-8 expression and tumor necrosis factor-induced IL-8 expression (P < 0.05 for both), yet NF-κB activity was not dependent on Src. We therefore suggest that Src activation, through phosphorylation of␣STAT3, and NF-κB are all required for expression of IL-8 a critical angiogenic-promoting factor in pancreatic adenocarcinomas. Angiogenesis (dpeaa)DE-He213 IL-8 (dpeaa)DE-He213 Src (dpeaa)DE-He213 NF-κB (dpeaa)DE-He213 STAT3 (dpeaa)DE-He213 NF-kappaB (dpeaa)DE-He213 Pancreatic adenocarcinoma (dpeaa)DE-He213 Gray, Michael J. verfasserin aut Nawrocki, Steffan T. verfasserin aut Summy, Justin M. verfasserin aut Lesslie, Donald P. verfasserin aut Evans, Douglas B. verfasserin aut Sawyer, Tomi K. verfasserin aut Shakespeare, William C. verfasserin aut Watowich, Stephanie S. verfasserin aut Chiao, Paul J. verfasserin aut McConkey, David J. verfasserin aut Gallick, Gary E. verfasserin aut Enthalten in Angiogenesis Dordrecht [u.a.] : Springer Science + Business Media B.V, 1997 9(2006), 2 vom: Juni, Seite 101-110 (DE-627)320427889 (DE-600)2003393-X 1573-7209 nnns volume:9 year:2006 number:2 month:06 pages:101-110 https://dx.doi.org/10.1007/s10456-006-9038-9 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_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 44.85 ASE AR 9 2006 2 06 101-110 |
| spelling |
10.1007/s10456-006-9038-9 doi (DE-627)SPR010159835 (SPR)s10456-006-9038-9-e DE-627 ger DE-627 rakwb eng 610 ASE 44.85 bkl Trevino, Jose G. verfasserin aut Src activation of Stat3 is an independent requirement from NF-κB activation for constitutive IL-8 expression in human pancreatic adenocarcinoma cells 2006 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Human pancreatic tumors often overexpress the angiogenesis-promoting factor Interleukin 8 (IL-8), in part due to overexpression of NF-κB, a frequent occurrence in pancreatic adenocarcinoma. In this study, we demonstrate that reducing c-Src kinase activity, through either pharmacologic inhibition or small interfering RNA-targeted reduction of Src expression, significantly decreased IL-8 expression (P < 0.05) without affecting NF-κB-mediated transcription, but by decreasing phosphorylation of STAT3. To ascertain whether Src-mediated expression of IL-8 was dependent on STAT3, we used stable clones expressing a dominant-negative isoform of STAT3 that inhibits endogenous STAT3 phosphorylation and subsequent DNA binding and STAT3-mediated gene expression or a constitutively activated isoform of STAT3. IL-8 expression was significantly lower in clones expressing the dominant-negative isoform and significantly increased in clones expressing the activated isoform (P < 0.05 for both). Pharmacologic inhibition of NF-κB activity significantly reduced basal IL-8 expression and tumor necrosis factor-induced IL-8 expression (P < 0.05 for both), yet NF-κB activity was not dependent on Src. We therefore suggest that Src activation, through phosphorylation of␣STAT3, and NF-κB are all required for expression of IL-8 a critical angiogenic-promoting factor in pancreatic adenocarcinomas. Angiogenesis (dpeaa)DE-He213 IL-8 (dpeaa)DE-He213 Src (dpeaa)DE-He213 NF-κB (dpeaa)DE-He213 STAT3 (dpeaa)DE-He213 NF-kappaB (dpeaa)DE-He213 Pancreatic adenocarcinoma (dpeaa)DE-He213 Gray, Michael J. verfasserin aut Nawrocki, Steffan T. verfasserin aut Summy, Justin M. verfasserin aut Lesslie, Donald P. verfasserin aut Evans, Douglas B. verfasserin aut Sawyer, Tomi K. verfasserin aut Shakespeare, William C. verfasserin aut Watowich, Stephanie S. verfasserin aut Chiao, Paul J. verfasserin aut McConkey, David J. verfasserin aut Gallick, Gary E. verfasserin aut Enthalten in Angiogenesis Dordrecht [u.a.] : Springer Science + Business Media B.V, 1997 9(2006), 2 vom: Juni, Seite 101-110 (DE-627)320427889 (DE-600)2003393-X 1573-7209 nnns volume:9 year:2006 number:2 month:06 pages:101-110 https://dx.doi.org/10.1007/s10456-006-9038-9 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_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 44.85 ASE AR 9 2006 2 06 101-110 |
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10.1007/s10456-006-9038-9 doi (DE-627)SPR010159835 (SPR)s10456-006-9038-9-e DE-627 ger DE-627 rakwb eng 610 ASE 44.85 bkl Trevino, Jose G. verfasserin aut Src activation of Stat3 is an independent requirement from NF-κB activation for constitutive IL-8 expression in human pancreatic adenocarcinoma cells 2006 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Human pancreatic tumors often overexpress the angiogenesis-promoting factor Interleukin 8 (IL-8), in part due to overexpression of NF-κB, a frequent occurrence in pancreatic adenocarcinoma. In this study, we demonstrate that reducing c-Src kinase activity, through either pharmacologic inhibition or small interfering RNA-targeted reduction of Src expression, significantly decreased IL-8 expression (P < 0.05) without affecting NF-κB-mediated transcription, but by decreasing phosphorylation of STAT3. To ascertain whether Src-mediated expression of IL-8 was dependent on STAT3, we used stable clones expressing a dominant-negative isoform of STAT3 that inhibits endogenous STAT3 phosphorylation and subsequent DNA binding and STAT3-mediated gene expression or a constitutively activated isoform of STAT3. IL-8 expression was significantly lower in clones expressing the dominant-negative isoform and significantly increased in clones expressing the activated isoform (P < 0.05 for both). Pharmacologic inhibition of NF-κB activity significantly reduced basal IL-8 expression and tumor necrosis factor-induced IL-8 expression (P < 0.05 for both), yet NF-κB activity was not dependent on Src. We therefore suggest that Src activation, through phosphorylation of␣STAT3, and NF-κB are all required for expression of IL-8 a critical angiogenic-promoting factor in pancreatic adenocarcinomas. Angiogenesis (dpeaa)DE-He213 IL-8 (dpeaa)DE-He213 Src (dpeaa)DE-He213 NF-κB (dpeaa)DE-He213 STAT3 (dpeaa)DE-He213 NF-kappaB (dpeaa)DE-He213 Pancreatic adenocarcinoma (dpeaa)DE-He213 Gray, Michael J. verfasserin aut Nawrocki, Steffan T. verfasserin aut Summy, Justin M. verfasserin aut Lesslie, Donald P. verfasserin aut Evans, Douglas B. verfasserin aut Sawyer, Tomi K. verfasserin aut Shakespeare, William C. verfasserin aut Watowich, Stephanie S. verfasserin aut Chiao, Paul J. verfasserin aut McConkey, David J. verfasserin aut Gallick, Gary E. verfasserin aut Enthalten in Angiogenesis Dordrecht [u.a.] : Springer Science + Business Media B.V, 1997 9(2006), 2 vom: Juni, Seite 101-110 (DE-627)320427889 (DE-600)2003393-X 1573-7209 nnns volume:9 year:2006 number:2 month:06 pages:101-110 https://dx.doi.org/10.1007/s10456-006-9038-9 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_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 44.85 ASE AR 9 2006 2 06 101-110 |
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10.1007/s10456-006-9038-9 doi (DE-627)SPR010159835 (SPR)s10456-006-9038-9-e DE-627 ger DE-627 rakwb eng 610 ASE 44.85 bkl Trevino, Jose G. verfasserin aut Src activation of Stat3 is an independent requirement from NF-κB activation for constitutive IL-8 expression in human pancreatic adenocarcinoma cells 2006 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Human pancreatic tumors often overexpress the angiogenesis-promoting factor Interleukin 8 (IL-8), in part due to overexpression of NF-κB, a frequent occurrence in pancreatic adenocarcinoma. In this study, we demonstrate that reducing c-Src kinase activity, through either pharmacologic inhibition or small interfering RNA-targeted reduction of Src expression, significantly decreased IL-8 expression (P < 0.05) without affecting NF-κB-mediated transcription, but by decreasing phosphorylation of STAT3. To ascertain whether Src-mediated expression of IL-8 was dependent on STAT3, we used stable clones expressing a dominant-negative isoform of STAT3 that inhibits endogenous STAT3 phosphorylation and subsequent DNA binding and STAT3-mediated gene expression or a constitutively activated isoform of STAT3. IL-8 expression was significantly lower in clones expressing the dominant-negative isoform and significantly increased in clones expressing the activated isoform (P < 0.05 for both). Pharmacologic inhibition of NF-κB activity significantly reduced basal IL-8 expression and tumor necrosis factor-induced IL-8 expression (P < 0.05 for both), yet NF-κB activity was not dependent on Src. We therefore suggest that Src activation, through phosphorylation of␣STAT3, and NF-κB are all required for expression of IL-8 a critical angiogenic-promoting factor in pancreatic adenocarcinomas. Angiogenesis (dpeaa)DE-He213 IL-8 (dpeaa)DE-He213 Src (dpeaa)DE-He213 NF-κB (dpeaa)DE-He213 STAT3 (dpeaa)DE-He213 NF-kappaB (dpeaa)DE-He213 Pancreatic adenocarcinoma (dpeaa)DE-He213 Gray, Michael J. verfasserin aut Nawrocki, Steffan T. verfasserin aut Summy, Justin M. verfasserin aut Lesslie, Donald P. verfasserin aut Evans, Douglas B. verfasserin aut Sawyer, Tomi K. verfasserin aut Shakespeare, William C. verfasserin aut Watowich, Stephanie S. verfasserin aut Chiao, Paul J. verfasserin aut McConkey, David J. verfasserin aut Gallick, Gary E. verfasserin aut Enthalten in Angiogenesis Dordrecht [u.a.] : Springer Science + Business Media B.V, 1997 9(2006), 2 vom: Juni, Seite 101-110 (DE-627)320427889 (DE-600)2003393-X 1573-7209 nnns volume:9 year:2006 number:2 month:06 pages:101-110 https://dx.doi.org/10.1007/s10456-006-9038-9 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_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 44.85 ASE AR 9 2006 2 06 101-110 |
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10.1007/s10456-006-9038-9 doi (DE-627)SPR010159835 (SPR)s10456-006-9038-9-e DE-627 ger DE-627 rakwb eng 610 ASE 44.85 bkl Trevino, Jose G. verfasserin aut Src activation of Stat3 is an independent requirement from NF-κB activation for constitutive IL-8 expression in human pancreatic adenocarcinoma cells 2006 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Human pancreatic tumors often overexpress the angiogenesis-promoting factor Interleukin 8 (IL-8), in part due to overexpression of NF-κB, a frequent occurrence in pancreatic adenocarcinoma. In this study, we demonstrate that reducing c-Src kinase activity, through either pharmacologic inhibition or small interfering RNA-targeted reduction of Src expression, significantly decreased IL-8 expression (P < 0.05) without affecting NF-κB-mediated transcription, but by decreasing phosphorylation of STAT3. To ascertain whether Src-mediated expression of IL-8 was dependent on STAT3, we used stable clones expressing a dominant-negative isoform of STAT3 that inhibits endogenous STAT3 phosphorylation and subsequent DNA binding and STAT3-mediated gene expression or a constitutively activated isoform of STAT3. IL-8 expression was significantly lower in clones expressing the dominant-negative isoform and significantly increased in clones expressing the activated isoform (P < 0.05 for both). Pharmacologic inhibition of NF-κB activity significantly reduced basal IL-8 expression and tumor necrosis factor-induced IL-8 expression (P < 0.05 for both), yet NF-κB activity was not dependent on Src. We therefore suggest that Src activation, through phosphorylation of␣STAT3, and NF-κB are all required for expression of IL-8 a critical angiogenic-promoting factor in pancreatic adenocarcinomas. Angiogenesis (dpeaa)DE-He213 IL-8 (dpeaa)DE-He213 Src (dpeaa)DE-He213 NF-κB (dpeaa)DE-He213 STAT3 (dpeaa)DE-He213 NF-kappaB (dpeaa)DE-He213 Pancreatic adenocarcinoma (dpeaa)DE-He213 Gray, Michael J. verfasserin aut Nawrocki, Steffan T. verfasserin aut Summy, Justin M. verfasserin aut Lesslie, Donald P. verfasserin aut Evans, Douglas B. verfasserin aut Sawyer, Tomi K. verfasserin aut Shakespeare, William C. verfasserin aut Watowich, Stephanie S. verfasserin aut Chiao, Paul J. verfasserin aut McConkey, David J. verfasserin aut Gallick, Gary E. verfasserin aut Enthalten in Angiogenesis Dordrecht [u.a.] : Springer Science + Business Media B.V, 1997 9(2006), 2 vom: Juni, Seite 101-110 (DE-627)320427889 (DE-600)2003393-X 1573-7209 nnns volume:9 year:2006 number:2 month:06 pages:101-110 https://dx.doi.org/10.1007/s10456-006-9038-9 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_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 44.85 ASE AR 9 2006 2 06 101-110 |
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Enthalten in Angiogenesis 9(2006), 2 vom: Juni, Seite 101-110 volume:9 year:2006 number:2 month:06 pages:101-110 |
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Angiogenesis IL-8 Src NF-κB STAT3 NF-kappaB Pancreatic adenocarcinoma |
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Trevino, Jose G. @@aut@@ Gray, Michael J. @@aut@@ Nawrocki, Steffan T. @@aut@@ Summy, Justin M. @@aut@@ Lesslie, Donald P. @@aut@@ Evans, Douglas B. @@aut@@ Sawyer, Tomi K. @@aut@@ Shakespeare, William C. @@aut@@ Watowich, Stephanie S. @@aut@@ Chiao, Paul J. @@aut@@ McConkey, David J. @@aut@@ Gallick, Gary E. @@aut@@ |
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In this study, we demonstrate that reducing c-Src kinase activity, through either pharmacologic inhibition or small interfering RNA-targeted reduction of Src expression, significantly decreased IL-8 expression (P < 0.05) without affecting NF-κB-mediated transcription, but by decreasing phosphorylation of STAT3. To ascertain whether Src-mediated expression of IL-8 was dependent on STAT3, we used stable clones expressing a dominant-negative isoform of STAT3 that inhibits endogenous STAT3 phosphorylation and subsequent DNA binding and STAT3-mediated gene expression or a constitutively activated isoform of STAT3. IL-8 expression was significantly lower in clones expressing the dominant-negative isoform and significantly increased in clones expressing the activated isoform (P < 0.05 for both). Pharmacologic inhibition of NF-κB activity significantly reduced basal IL-8 expression and tumor necrosis factor-induced IL-8 expression (P < 0.05 for both), yet NF-κB activity was not dependent on Src. 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| author |
Trevino, Jose G. |
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Trevino, Jose G. ddc 610 bkl 44.85 misc Angiogenesis misc IL-8 misc Src misc NF-κB misc STAT3 misc NF-kappaB misc Pancreatic adenocarcinoma Src activation of Stat3 is an independent requirement from NF-κB activation for constitutive IL-8 expression in human pancreatic adenocarcinoma cells |
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610 ASE 44.85 bkl Src activation of Stat3 is an independent requirement from NF-κB activation for constitutive IL-8 expression in human pancreatic adenocarcinoma cells Angiogenesis (dpeaa)DE-He213 IL-8 (dpeaa)DE-He213 Src (dpeaa)DE-He213 NF-κB (dpeaa)DE-He213 STAT3 (dpeaa)DE-He213 NF-kappaB (dpeaa)DE-He213 Pancreatic adenocarcinoma (dpeaa)DE-He213 |
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ddc 610 bkl 44.85 misc Angiogenesis misc IL-8 misc Src misc NF-κB misc STAT3 misc NF-kappaB misc Pancreatic adenocarcinoma |
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ddc 610 bkl 44.85 misc Angiogenesis misc IL-8 misc Src misc NF-κB misc STAT3 misc NF-kappaB misc Pancreatic adenocarcinoma |
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ddc 610 bkl 44.85 misc Angiogenesis misc IL-8 misc Src misc NF-κB misc STAT3 misc NF-kappaB misc Pancreatic adenocarcinoma |
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Src activation of Stat3 is an independent requirement from NF-κB activation for constitutive IL-8 expression in human pancreatic adenocarcinoma cells |
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(DE-627)SPR010159835 (SPR)s10456-006-9038-9-e |
| title_full |
Src activation of Stat3 is an independent requirement from NF-κB activation for constitutive IL-8 expression in human pancreatic adenocarcinoma cells |
| author_sort |
Trevino, Jose G. |
| journal |
Angiogenesis |
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Angiogenesis |
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eng |
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600 - Technology |
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marc |
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2006 |
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101 |
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Trevino, Jose G. Gray, Michael J. Nawrocki, Steffan T. Summy, Justin M. Lesslie, Donald P. Evans, Douglas B. Sawyer, Tomi K. Shakespeare, William C. Watowich, Stephanie S. Chiao, Paul J. McConkey, David J. Gallick, Gary E. |
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9 |
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610 ASE 44.85 bkl |
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Elektronische Aufsätze |
| author-letter |
Trevino, Jose G. |
| doi_str_mv |
10.1007/s10456-006-9038-9 |
| dewey-full |
610 |
| author2-role |
verfasserin |
| title_sort |
src activation of stat3 is an independent requirement from nf-κb activation for constitutive il-8 expression in human pancreatic adenocarcinoma cells |
| title_auth |
Src activation of Stat3 is an independent requirement from NF-κB activation for constitutive IL-8 expression in human pancreatic adenocarcinoma cells |
| abstract |
Abstract Human pancreatic tumors often overexpress the angiogenesis-promoting factor Interleukin 8 (IL-8), in part due to overexpression of NF-κB, a frequent occurrence in pancreatic adenocarcinoma. In this study, we demonstrate that reducing c-Src kinase activity, through either pharmacologic inhibition or small interfering RNA-targeted reduction of Src expression, significantly decreased IL-8 expression (P < 0.05) without affecting NF-κB-mediated transcription, but by decreasing phosphorylation of STAT3. To ascertain whether Src-mediated expression of IL-8 was dependent on STAT3, we used stable clones expressing a dominant-negative isoform of STAT3 that inhibits endogenous STAT3 phosphorylation and subsequent DNA binding and STAT3-mediated gene expression or a constitutively activated isoform of STAT3. IL-8 expression was significantly lower in clones expressing the dominant-negative isoform and significantly increased in clones expressing the activated isoform (P < 0.05 for both). Pharmacologic inhibition of NF-κB activity significantly reduced basal IL-8 expression and tumor necrosis factor-induced IL-8 expression (P < 0.05 for both), yet NF-κB activity was not dependent on Src. We therefore suggest that Src activation, through phosphorylation of␣STAT3, and NF-κB are all required for expression of IL-8 a critical angiogenic-promoting factor in pancreatic adenocarcinomas. |
| abstractGer |
Abstract Human pancreatic tumors often overexpress the angiogenesis-promoting factor Interleukin 8 (IL-8), in part due to overexpression of NF-κB, a frequent occurrence in pancreatic adenocarcinoma. In this study, we demonstrate that reducing c-Src kinase activity, through either pharmacologic inhibition or small interfering RNA-targeted reduction of Src expression, significantly decreased IL-8 expression (P < 0.05) without affecting NF-κB-mediated transcription, but by decreasing phosphorylation of STAT3. To ascertain whether Src-mediated expression of IL-8 was dependent on STAT3, we used stable clones expressing a dominant-negative isoform of STAT3 that inhibits endogenous STAT3 phosphorylation and subsequent DNA binding and STAT3-mediated gene expression or a constitutively activated isoform of STAT3. IL-8 expression was significantly lower in clones expressing the dominant-negative isoform and significantly increased in clones expressing the activated isoform (P < 0.05 for both). Pharmacologic inhibition of NF-κB activity significantly reduced basal IL-8 expression and tumor necrosis factor-induced IL-8 expression (P < 0.05 for both), yet NF-κB activity was not dependent on Src. We therefore suggest that Src activation, through phosphorylation of␣STAT3, and NF-κB are all required for expression of IL-8 a critical angiogenic-promoting factor in pancreatic adenocarcinomas. |
| abstract_unstemmed |
Abstract Human pancreatic tumors often overexpress the angiogenesis-promoting factor Interleukin 8 (IL-8), in part due to overexpression of NF-κB, a frequent occurrence in pancreatic adenocarcinoma. In this study, we demonstrate that reducing c-Src kinase activity, through either pharmacologic inhibition or small interfering RNA-targeted reduction of Src expression, significantly decreased IL-8 expression (P < 0.05) without affecting NF-κB-mediated transcription, but by decreasing phosphorylation of STAT3. To ascertain whether Src-mediated expression of IL-8 was dependent on STAT3, we used stable clones expressing a dominant-negative isoform of STAT3 that inhibits endogenous STAT3 phosphorylation and subsequent DNA binding and STAT3-mediated gene expression or a constitutively activated isoform of STAT3. IL-8 expression was significantly lower in clones expressing the dominant-negative isoform and significantly increased in clones expressing the activated isoform (P < 0.05 for both). Pharmacologic inhibition of NF-κB activity significantly reduced basal IL-8 expression and tumor necrosis factor-induced IL-8 expression (P < 0.05 for both), yet NF-κB activity was not dependent on Src. We therefore suggest that Src activation, through phosphorylation of␣STAT3, and NF-κB are all required for expression of IL-8 a critical angiogenic-promoting factor in pancreatic adenocarcinomas. |
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2 |
| title_short |
Src activation of Stat3 is an independent requirement from NF-κB activation for constitutive IL-8 expression in human pancreatic adenocarcinoma cells |
| url |
https://dx.doi.org/10.1007/s10456-006-9038-9 |
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| author2 |
Gray, Michael J. Nawrocki, Steffan T. Summy, Justin M. Lesslie, Donald P. Evans, Douglas B. Sawyer, Tomi K. Shakespeare, William C. Watowich, Stephanie S. Chiao, Paul J. McConkey, David J. Gallick, Gary E. |
| author2Str |
Gray, Michael J. Nawrocki, Steffan T. Summy, Justin M. Lesslie, Donald P. Evans, Douglas B. Sawyer, Tomi K. Shakespeare, William C. Watowich, Stephanie S. Chiao, Paul J. McConkey, David J. Gallick, Gary E. |
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| up_date |
2024-07-03T14:18:45.474Z |
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| score |
7.402648 |