Anticancer Effect of Celecoxib via COX-2 Dependent and Independent Mechanisms in Human Gastric Cancers Cells
Abstract Cyclooxygenase-2 (COX-2) inhibitors cause growth inhibition of human gastric carcinoma cells, but it remains unclear whether this is both COX-2 dependent and independent. The related mechanisms remain to be determined. Both low COX-2 expressing gastric carcinoma and high COX-2 expressing ga...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Liu, Hua [verfasserIn] Huang, Peixin [verfasserIn] Xu, Xuanfu [verfasserIn] Liu, Jun [verfasserIn] Guo, Chuanyong [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2008 |
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| Schlagwörter: |
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| Übergeordnetes Werk: |
Enthalten in: Digestive diseases and sciences - Dordrecht : Springer Science + Business Media B.V., 1934, 54(2008), 7 vom: 16. Okt., Seite 1418-1424 |
|---|---|
| Übergeordnetes Werk: |
volume:54 ; year:2008 ; number:7 ; day:16 ; month:10 ; pages:1418-1424 |
| Links: |
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| DOI / URN: |
10.1007/s10620-008-0510-9 |
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| Katalog-ID: |
SPR011850051 |
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| 245 | 1 | 0 | |a Anticancer Effect of Celecoxib via COX-2 Dependent and Independent Mechanisms in Human Gastric Cancers Cells |
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| 520 | |a Abstract Cyclooxygenase-2 (COX-2) inhibitors cause growth inhibition of human gastric carcinoma cells, but it remains unclear whether this is both COX-2 dependent and independent. The related mechanisms remain to be determined. Both low COX-2 expressing gastric carcinoma and high COX-2 expressing gastric carcinoma cells were used to study the effect and mechanisms of celecoxib on gastric carcinoma cell growth. Celecoxib resulted in comparable growth inhibition in AGS cells with stable transfections of small interfering RNA (siRNA) against COX-2 (SAC) and negative control vector (NC) cells. Simultaneously, celecoxib resulted in significant reduction of Bcl-2 and significant increase of $ p21^{WAF1} $ and $ p27^{KIP1} $ in SAC and NC cells. The present study shows that celecoxib causes growth inhibition of gastric carcinoma cells by decreasing Bcl-2 of cyclooxygenase-2-dependent pathway, and by increasing $ p21^{WAF1} $ and $ p27^{KIP1} $ of cyclooxygenase-2-independent pathway. These data extend our knowledge on the effect and mechanisms of celecoxib-induced inhibition of gastric carcinoma cell growth. | ||
| 650 | 4 | |a Gastric carcinoma |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Cyclooxygenase-2 |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a RNA interference |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Cyclooxygenase-2-dependent pathway |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Cyclooxygenase-2-independent pathway |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Huang, Peixin |e verfasserin |4 aut | |
| 700 | 1 | |a Xu, Xuanfu |e verfasserin |4 aut | |
| 700 | 1 | |a Liu, Jun |e verfasserin |4 aut | |
| 700 | 1 | |a Guo, Chuanyong |e verfasserin |4 aut | |
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| allfields |
10.1007/s10620-008-0510-9 doi (DE-627)SPR011850051 (SPR)s10620-008-0510-9-e DE-627 ger DE-627 rakwb eng 610 ASE 610 ASE 44.87 bkl Liu, Hua verfasserin aut Anticancer Effect of Celecoxib via COX-2 Dependent and Independent Mechanisms in Human Gastric Cancers Cells 2008 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Cyclooxygenase-2 (COX-2) inhibitors cause growth inhibition of human gastric carcinoma cells, but it remains unclear whether this is both COX-2 dependent and independent. The related mechanisms remain to be determined. Both low COX-2 expressing gastric carcinoma and high COX-2 expressing gastric carcinoma cells were used to study the effect and mechanisms of celecoxib on gastric carcinoma cell growth. Celecoxib resulted in comparable growth inhibition in AGS cells with stable transfections of small interfering RNA (siRNA) against COX-2 (SAC) and negative control vector (NC) cells. Simultaneously, celecoxib resulted in significant reduction of Bcl-2 and significant increase of $ p21^{WAF1} $ and $ p27^{KIP1} $ in SAC and NC cells. The present study shows that celecoxib causes growth inhibition of gastric carcinoma cells by decreasing Bcl-2 of cyclooxygenase-2-dependent pathway, and by increasing $ p21^{WAF1} $ and $ p27^{KIP1} $ of cyclooxygenase-2-independent pathway. These data extend our knowledge on the effect and mechanisms of celecoxib-induced inhibition of gastric carcinoma cell growth. Gastric carcinoma (dpeaa)DE-He213 Cyclooxygenase-2 (dpeaa)DE-He213 RNA interference (dpeaa)DE-He213 Cyclooxygenase-2-dependent pathway (dpeaa)DE-He213 Cyclooxygenase-2-independent pathway (dpeaa)DE-He213 Huang, Peixin verfasserin aut Xu, Xuanfu verfasserin aut Liu, Jun verfasserin aut Guo, Chuanyong verfasserin aut Enthalten in Digestive diseases and sciences Dordrecht : Springer Science + Business Media B.V., 1934 54(2008), 7 vom: 16. Okt., Seite 1418-1424 (DE-627)320525384 (DE-600)2015102-0 1573-2568 nnns volume:54 year:2008 number:7 day:16 month:10 pages:1418-1424 https://dx.doi.org/10.1007/s10620-008-0510-9 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_152 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_267 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 44.87 ASE AR 54 2008 7 16 10 1418-1424 |
| spelling |
10.1007/s10620-008-0510-9 doi (DE-627)SPR011850051 (SPR)s10620-008-0510-9-e DE-627 ger DE-627 rakwb eng 610 ASE 610 ASE 44.87 bkl Liu, Hua verfasserin aut Anticancer Effect of Celecoxib via COX-2 Dependent and Independent Mechanisms in Human Gastric Cancers Cells 2008 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Cyclooxygenase-2 (COX-2) inhibitors cause growth inhibition of human gastric carcinoma cells, but it remains unclear whether this is both COX-2 dependent and independent. The related mechanisms remain to be determined. Both low COX-2 expressing gastric carcinoma and high COX-2 expressing gastric carcinoma cells were used to study the effect and mechanisms of celecoxib on gastric carcinoma cell growth. Celecoxib resulted in comparable growth inhibition in AGS cells with stable transfections of small interfering RNA (siRNA) against COX-2 (SAC) and negative control vector (NC) cells. Simultaneously, celecoxib resulted in significant reduction of Bcl-2 and significant increase of $ p21^{WAF1} $ and $ p27^{KIP1} $ in SAC and NC cells. The present study shows that celecoxib causes growth inhibition of gastric carcinoma cells by decreasing Bcl-2 of cyclooxygenase-2-dependent pathway, and by increasing $ p21^{WAF1} $ and $ p27^{KIP1} $ of cyclooxygenase-2-independent pathway. These data extend our knowledge on the effect and mechanisms of celecoxib-induced inhibition of gastric carcinoma cell growth. Gastric carcinoma (dpeaa)DE-He213 Cyclooxygenase-2 (dpeaa)DE-He213 RNA interference (dpeaa)DE-He213 Cyclooxygenase-2-dependent pathway (dpeaa)DE-He213 Cyclooxygenase-2-independent pathway (dpeaa)DE-He213 Huang, Peixin verfasserin aut Xu, Xuanfu verfasserin aut Liu, Jun verfasserin aut Guo, Chuanyong verfasserin aut Enthalten in Digestive diseases and sciences Dordrecht : Springer Science + Business Media B.V., 1934 54(2008), 7 vom: 16. Okt., Seite 1418-1424 (DE-627)320525384 (DE-600)2015102-0 1573-2568 nnns volume:54 year:2008 number:7 day:16 month:10 pages:1418-1424 https://dx.doi.org/10.1007/s10620-008-0510-9 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_152 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_267 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 44.87 ASE AR 54 2008 7 16 10 1418-1424 |
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10.1007/s10620-008-0510-9 doi (DE-627)SPR011850051 (SPR)s10620-008-0510-9-e DE-627 ger DE-627 rakwb eng 610 ASE 610 ASE 44.87 bkl Liu, Hua verfasserin aut Anticancer Effect of Celecoxib via COX-2 Dependent and Independent Mechanisms in Human Gastric Cancers Cells 2008 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Cyclooxygenase-2 (COX-2) inhibitors cause growth inhibition of human gastric carcinoma cells, but it remains unclear whether this is both COX-2 dependent and independent. The related mechanisms remain to be determined. Both low COX-2 expressing gastric carcinoma and high COX-2 expressing gastric carcinoma cells were used to study the effect and mechanisms of celecoxib on gastric carcinoma cell growth. Celecoxib resulted in comparable growth inhibition in AGS cells with stable transfections of small interfering RNA (siRNA) against COX-2 (SAC) and negative control vector (NC) cells. Simultaneously, celecoxib resulted in significant reduction of Bcl-2 and significant increase of $ p21^{WAF1} $ and $ p27^{KIP1} $ in SAC and NC cells. The present study shows that celecoxib causes growth inhibition of gastric carcinoma cells by decreasing Bcl-2 of cyclooxygenase-2-dependent pathway, and by increasing $ p21^{WAF1} $ and $ p27^{KIP1} $ of cyclooxygenase-2-independent pathway. These data extend our knowledge on the effect and mechanisms of celecoxib-induced inhibition of gastric carcinoma cell growth. Gastric carcinoma (dpeaa)DE-He213 Cyclooxygenase-2 (dpeaa)DE-He213 RNA interference (dpeaa)DE-He213 Cyclooxygenase-2-dependent pathway (dpeaa)DE-He213 Cyclooxygenase-2-independent pathway (dpeaa)DE-He213 Huang, Peixin verfasserin aut Xu, Xuanfu verfasserin aut Liu, Jun verfasserin aut Guo, Chuanyong verfasserin aut Enthalten in Digestive diseases and sciences Dordrecht : Springer Science + Business Media B.V., 1934 54(2008), 7 vom: 16. Okt., Seite 1418-1424 (DE-627)320525384 (DE-600)2015102-0 1573-2568 nnns volume:54 year:2008 number:7 day:16 month:10 pages:1418-1424 https://dx.doi.org/10.1007/s10620-008-0510-9 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_152 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_267 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 44.87 ASE AR 54 2008 7 16 10 1418-1424 |
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10.1007/s10620-008-0510-9 doi (DE-627)SPR011850051 (SPR)s10620-008-0510-9-e DE-627 ger DE-627 rakwb eng 610 ASE 610 ASE 44.87 bkl Liu, Hua verfasserin aut Anticancer Effect of Celecoxib via COX-2 Dependent and Independent Mechanisms in Human Gastric Cancers Cells 2008 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Cyclooxygenase-2 (COX-2) inhibitors cause growth inhibition of human gastric carcinoma cells, but it remains unclear whether this is both COX-2 dependent and independent. The related mechanisms remain to be determined. Both low COX-2 expressing gastric carcinoma and high COX-2 expressing gastric carcinoma cells were used to study the effect and mechanisms of celecoxib on gastric carcinoma cell growth. Celecoxib resulted in comparable growth inhibition in AGS cells with stable transfections of small interfering RNA (siRNA) against COX-2 (SAC) and negative control vector (NC) cells. Simultaneously, celecoxib resulted in significant reduction of Bcl-2 and significant increase of $ p21^{WAF1} $ and $ p27^{KIP1} $ in SAC and NC cells. The present study shows that celecoxib causes growth inhibition of gastric carcinoma cells by decreasing Bcl-2 of cyclooxygenase-2-dependent pathway, and by increasing $ p21^{WAF1} $ and $ p27^{KIP1} $ of cyclooxygenase-2-independent pathway. These data extend our knowledge on the effect and mechanisms of celecoxib-induced inhibition of gastric carcinoma cell growth. Gastric carcinoma (dpeaa)DE-He213 Cyclooxygenase-2 (dpeaa)DE-He213 RNA interference (dpeaa)DE-He213 Cyclooxygenase-2-dependent pathway (dpeaa)DE-He213 Cyclooxygenase-2-independent pathway (dpeaa)DE-He213 Huang, Peixin verfasserin aut Xu, Xuanfu verfasserin aut Liu, Jun verfasserin aut Guo, Chuanyong verfasserin aut Enthalten in Digestive diseases and sciences Dordrecht : Springer Science + Business Media B.V., 1934 54(2008), 7 vom: 16. Okt., Seite 1418-1424 (DE-627)320525384 (DE-600)2015102-0 1573-2568 nnns volume:54 year:2008 number:7 day:16 month:10 pages:1418-1424 https://dx.doi.org/10.1007/s10620-008-0510-9 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_152 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_267 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 44.87 ASE AR 54 2008 7 16 10 1418-1424 |
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10.1007/s10620-008-0510-9 doi (DE-627)SPR011850051 (SPR)s10620-008-0510-9-e DE-627 ger DE-627 rakwb eng 610 ASE 610 ASE 44.87 bkl Liu, Hua verfasserin aut Anticancer Effect of Celecoxib via COX-2 Dependent and Independent Mechanisms in Human Gastric Cancers Cells 2008 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Cyclooxygenase-2 (COX-2) inhibitors cause growth inhibition of human gastric carcinoma cells, but it remains unclear whether this is both COX-2 dependent and independent. The related mechanisms remain to be determined. Both low COX-2 expressing gastric carcinoma and high COX-2 expressing gastric carcinoma cells were used to study the effect and mechanisms of celecoxib on gastric carcinoma cell growth. Celecoxib resulted in comparable growth inhibition in AGS cells with stable transfections of small interfering RNA (siRNA) against COX-2 (SAC) and negative control vector (NC) cells. Simultaneously, celecoxib resulted in significant reduction of Bcl-2 and significant increase of $ p21^{WAF1} $ and $ p27^{KIP1} $ in SAC and NC cells. The present study shows that celecoxib causes growth inhibition of gastric carcinoma cells by decreasing Bcl-2 of cyclooxygenase-2-dependent pathway, and by increasing $ p21^{WAF1} $ and $ p27^{KIP1} $ of cyclooxygenase-2-independent pathway. These data extend our knowledge on the effect and mechanisms of celecoxib-induced inhibition of gastric carcinoma cell growth. Gastric carcinoma (dpeaa)DE-He213 Cyclooxygenase-2 (dpeaa)DE-He213 RNA interference (dpeaa)DE-He213 Cyclooxygenase-2-dependent pathway (dpeaa)DE-He213 Cyclooxygenase-2-independent pathway (dpeaa)DE-He213 Huang, Peixin verfasserin aut Xu, Xuanfu verfasserin aut Liu, Jun verfasserin aut Guo, Chuanyong verfasserin aut Enthalten in Digestive diseases and sciences Dordrecht : Springer Science + Business Media B.V., 1934 54(2008), 7 vom: 16. Okt., Seite 1418-1424 (DE-627)320525384 (DE-600)2015102-0 1573-2568 nnns volume:54 year:2008 number:7 day:16 month:10 pages:1418-1424 https://dx.doi.org/10.1007/s10620-008-0510-9 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_152 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_267 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 44.87 ASE AR 54 2008 7 16 10 1418-1424 |
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English |
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Enthalten in Digestive diseases and sciences 54(2008), 7 vom: 16. Okt., Seite 1418-1424 volume:54 year:2008 number:7 day:16 month:10 pages:1418-1424 |
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Enthalten in Digestive diseases and sciences 54(2008), 7 vom: 16. Okt., Seite 1418-1424 volume:54 year:2008 number:7 day:16 month:10 pages:1418-1424 |
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findex.gbv.de |
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Gastric carcinoma Cyclooxygenase-2 RNA interference Cyclooxygenase-2-dependent pathway Cyclooxygenase-2-independent pathway |
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Digestive diseases and sciences |
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Liu, Hua @@aut@@ Huang, Peixin @@aut@@ Xu, Xuanfu @@aut@@ Liu, Jun @@aut@@ Guo, Chuanyong @@aut@@ |
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2008-10-16T00:00:00Z |
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The related mechanisms remain to be determined. Both low COX-2 expressing gastric carcinoma and high COX-2 expressing gastric carcinoma cells were used to study the effect and mechanisms of celecoxib on gastric carcinoma cell growth. Celecoxib resulted in comparable growth inhibition in AGS cells with stable transfections of small interfering RNA (siRNA) against COX-2 (SAC) and negative control vector (NC) cells. Simultaneously, celecoxib resulted in significant reduction of Bcl-2 and significant increase of $ p21^{WAF1} $ and $ p27^{KIP1} $ in SAC and NC cells. The present study shows that celecoxib causes growth inhibition of gastric carcinoma cells by decreasing Bcl-2 of cyclooxygenase-2-dependent pathway, and by increasing $ p21^{WAF1} $ and $ p27^{KIP1} $ of cyclooxygenase-2-independent pathway. 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Liu, Hua |
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Liu, Hua ddc 610 bkl 44.87 misc Gastric carcinoma misc Cyclooxygenase-2 misc RNA interference misc Cyclooxygenase-2-dependent pathway misc Cyclooxygenase-2-independent pathway Anticancer Effect of Celecoxib via COX-2 Dependent and Independent Mechanisms in Human Gastric Cancers Cells |
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610 ASE 44.87 bkl Anticancer Effect of Celecoxib via COX-2 Dependent and Independent Mechanisms in Human Gastric Cancers Cells Gastric carcinoma (dpeaa)DE-He213 Cyclooxygenase-2 (dpeaa)DE-He213 RNA interference (dpeaa)DE-He213 Cyclooxygenase-2-dependent pathway (dpeaa)DE-He213 Cyclooxygenase-2-independent pathway (dpeaa)DE-He213 |
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anticancer effect of celecoxib via cox-2 dependent and independent mechanisms in human gastric cancers cells |
| title_auth |
Anticancer Effect of Celecoxib via COX-2 Dependent and Independent Mechanisms in Human Gastric Cancers Cells |
| abstract |
Abstract Cyclooxygenase-2 (COX-2) inhibitors cause growth inhibition of human gastric carcinoma cells, but it remains unclear whether this is both COX-2 dependent and independent. The related mechanisms remain to be determined. Both low COX-2 expressing gastric carcinoma and high COX-2 expressing gastric carcinoma cells were used to study the effect and mechanisms of celecoxib on gastric carcinoma cell growth. Celecoxib resulted in comparable growth inhibition in AGS cells with stable transfections of small interfering RNA (siRNA) against COX-2 (SAC) and negative control vector (NC) cells. Simultaneously, celecoxib resulted in significant reduction of Bcl-2 and significant increase of $ p21^{WAF1} $ and $ p27^{KIP1} $ in SAC and NC cells. The present study shows that celecoxib causes growth inhibition of gastric carcinoma cells by decreasing Bcl-2 of cyclooxygenase-2-dependent pathway, and by increasing $ p21^{WAF1} $ and $ p27^{KIP1} $ of cyclooxygenase-2-independent pathway. These data extend our knowledge on the effect and mechanisms of celecoxib-induced inhibition of gastric carcinoma cell growth. |
| abstractGer |
Abstract Cyclooxygenase-2 (COX-2) inhibitors cause growth inhibition of human gastric carcinoma cells, but it remains unclear whether this is both COX-2 dependent and independent. The related mechanisms remain to be determined. Both low COX-2 expressing gastric carcinoma and high COX-2 expressing gastric carcinoma cells were used to study the effect and mechanisms of celecoxib on gastric carcinoma cell growth. Celecoxib resulted in comparable growth inhibition in AGS cells with stable transfections of small interfering RNA (siRNA) against COX-2 (SAC) and negative control vector (NC) cells. Simultaneously, celecoxib resulted in significant reduction of Bcl-2 and significant increase of $ p21^{WAF1} $ and $ p27^{KIP1} $ in SAC and NC cells. The present study shows that celecoxib causes growth inhibition of gastric carcinoma cells by decreasing Bcl-2 of cyclooxygenase-2-dependent pathway, and by increasing $ p21^{WAF1} $ and $ p27^{KIP1} $ of cyclooxygenase-2-independent pathway. These data extend our knowledge on the effect and mechanisms of celecoxib-induced inhibition of gastric carcinoma cell growth. |
| abstract_unstemmed |
Abstract Cyclooxygenase-2 (COX-2) inhibitors cause growth inhibition of human gastric carcinoma cells, but it remains unclear whether this is both COX-2 dependent and independent. The related mechanisms remain to be determined. Both low COX-2 expressing gastric carcinoma and high COX-2 expressing gastric carcinoma cells were used to study the effect and mechanisms of celecoxib on gastric carcinoma cell growth. Celecoxib resulted in comparable growth inhibition in AGS cells with stable transfections of small interfering RNA (siRNA) against COX-2 (SAC) and negative control vector (NC) cells. Simultaneously, celecoxib resulted in significant reduction of Bcl-2 and significant increase of $ p21^{WAF1} $ and $ p27^{KIP1} $ in SAC and NC cells. The present study shows that celecoxib causes growth inhibition of gastric carcinoma cells by decreasing Bcl-2 of cyclooxygenase-2-dependent pathway, and by increasing $ p21^{WAF1} $ and $ p27^{KIP1} $ of cyclooxygenase-2-independent pathway. These data extend our knowledge on the effect and mechanisms of celecoxib-induced inhibition of gastric carcinoma cell growth. |
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| title_short |
Anticancer Effect of Celecoxib via COX-2 Dependent and Independent Mechanisms in Human Gastric Cancers Cells |
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https://dx.doi.org/10.1007/s10620-008-0510-9 |
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Huang, Peixin Xu, Xuanfu Liu, Jun Guo, Chuanyong |
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| doi_str |
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2024-07-04T00:41:40.288Z |
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| score |
7.4014244 |