Inhibitory effect of cucurbitacin E on pancreatic cancer cells growth via STAT3 signaling
Purpose Pancreatic cancer has been a serious disease worldwide for its high mortality. Cucurbitacin E is a member of triterpenoid family isolated from plants showing antiproliferative activity on various cancer cells. In this study, we have explored whether cucurbitacin E also has an anti-tumor effe...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Sun, Chunyan [verfasserIn] Zhang, Meixia [verfasserIn] Shan, Xiaolei [verfasserIn] Zhou, Xueying [verfasserIn] Yang, Jiao [verfasserIn] Wang, Yanli [verfasserIn] Li-Ling, Jesse [verfasserIn] Deng, Yihui [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2009 |
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| Schlagwörter: |
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| Übergeordnetes Werk: |
Enthalten in: Journal of cancer research and clinical oncology - Berlin : Springer, 1904, 136(2009), 4 vom: 09. Okt., Seite 603-610 |
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| Übergeordnetes Werk: |
volume:136 ; year:2009 ; number:4 ; day:09 ; month:10 ; pages:603-610 |
| Links: |
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| DOI / URN: |
10.1007/s00432-009-0698-x |
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| Katalog-ID: |
SPR005844525 |
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| 245 | 1 | 0 | |a Inhibitory effect of cucurbitacin E on pancreatic cancer cells growth via STAT3 signaling |
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| 520 | |a Purpose Pancreatic cancer has been a serious disease worldwide for its high mortality. Cucurbitacin E is a member of triterpenoid family isolated from plants showing antiproliferative activity on various cancer cells. In this study, we have explored whether cucurbitacin E also has an anti-tumor effect on pancreatic cancer cells. Methods Human pancreatic cancer cells PANC-1 were used to explore the effect and possible mechanisms of cucurbitacin E on cell cycle progression, apoptosis and proliferation. Results Cucurbitacin E has inhibited the growth of PANC-1 cells in a dose- and time-dependent manner, and has caused accumulation of cells at the $ G_{2} $/M phase as well as apoptosis. Western blotting also showed that cucurbitacin E treatment can inhibit STAT3 phosphorylation while upregulate p53 expression. Conclusions Our results suggested that cucurbitacin E may be an effective regimen for the chemotherapy of pancreatic cancer. | ||
| 650 | 4 | |a Cucurbitacin E |7 (dpeaa)DE-He213 | |
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| 650 | 4 | |a Pancreatic cancer |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a STAT3 |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Zhang, Meixia |e verfasserin |4 aut | |
| 700 | 1 | |a Shan, Xiaolei |e verfasserin |4 aut | |
| 700 | 1 | |a Zhou, Xueying |e verfasserin |4 aut | |
| 700 | 1 | |a Yang, Jiao |e verfasserin |4 aut | |
| 700 | 1 | |a Wang, Yanli |e verfasserin |4 aut | |
| 700 | 1 | |a Li-Ling, Jesse |e verfasserin |4 aut | |
| 700 | 1 | |a Deng, Yihui |e verfasserin |4 aut | |
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10.1007/s00432-009-0698-x doi (DE-627)SPR005844525 (SPR)s00432-009-0698-x-e DE-627 ger DE-627 rakwb eng 610 ASE 44.81 bkl Sun, Chunyan verfasserin aut Inhibitory effect of cucurbitacin E on pancreatic cancer cells growth via STAT3 signaling 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Purpose Pancreatic cancer has been a serious disease worldwide for its high mortality. Cucurbitacin E is a member of triterpenoid family isolated from plants showing antiproliferative activity on various cancer cells. In this study, we have explored whether cucurbitacin E also has an anti-tumor effect on pancreatic cancer cells. Methods Human pancreatic cancer cells PANC-1 were used to explore the effect and possible mechanisms of cucurbitacin E on cell cycle progression, apoptosis and proliferation. Results Cucurbitacin E has inhibited the growth of PANC-1 cells in a dose- and time-dependent manner, and has caused accumulation of cells at the $ G_{2} $/M phase as well as apoptosis. Western blotting also showed that cucurbitacin E treatment can inhibit STAT3 phosphorylation while upregulate p53 expression. Conclusions Our results suggested that cucurbitacin E may be an effective regimen for the chemotherapy of pancreatic cancer. Cucurbitacin E (dpeaa)DE-He213 p53 (dpeaa)DE-He213 PANC-1 (dpeaa)DE-He213 Pancreatic cancer (dpeaa)DE-He213 STAT3 (dpeaa)DE-He213 Zhang, Meixia verfasserin aut Shan, Xiaolei verfasserin aut Zhou, Xueying verfasserin aut Yang, Jiao verfasserin aut Wang, Yanli verfasserin aut Li-Ling, Jesse verfasserin aut Deng, Yihui verfasserin aut Enthalten in Journal of cancer research and clinical oncology Berlin : Springer, 1904 136(2009), 4 vom: 09. Okt., Seite 603-610 (DE-627)253769515 (DE-600)1459285-X 1432-1335 nnns volume:136 year:2009 number:4 day:09 month:10 pages:603-610 https://dx.doi.org/10.1007/s00432-009-0698-x 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_65 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_165 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_4328 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 136 2009 4 09 10 603-610 |
| spelling |
10.1007/s00432-009-0698-x doi (DE-627)SPR005844525 (SPR)s00432-009-0698-x-e DE-627 ger DE-627 rakwb eng 610 ASE 44.81 bkl Sun, Chunyan verfasserin aut Inhibitory effect of cucurbitacin E on pancreatic cancer cells growth via STAT3 signaling 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Purpose Pancreatic cancer has been a serious disease worldwide for its high mortality. Cucurbitacin E is a member of triterpenoid family isolated from plants showing antiproliferative activity on various cancer cells. In this study, we have explored whether cucurbitacin E also has an anti-tumor effect on pancreatic cancer cells. Methods Human pancreatic cancer cells PANC-1 were used to explore the effect and possible mechanisms of cucurbitacin E on cell cycle progression, apoptosis and proliferation. Results Cucurbitacin E has inhibited the growth of PANC-1 cells in a dose- and time-dependent manner, and has caused accumulation of cells at the $ G_{2} $/M phase as well as apoptosis. Western blotting also showed that cucurbitacin E treatment can inhibit STAT3 phosphorylation while upregulate p53 expression. Conclusions Our results suggested that cucurbitacin E may be an effective regimen for the chemotherapy of pancreatic cancer. Cucurbitacin E (dpeaa)DE-He213 p53 (dpeaa)DE-He213 PANC-1 (dpeaa)DE-He213 Pancreatic cancer (dpeaa)DE-He213 STAT3 (dpeaa)DE-He213 Zhang, Meixia verfasserin aut Shan, Xiaolei verfasserin aut Zhou, Xueying verfasserin aut Yang, Jiao verfasserin aut Wang, Yanli verfasserin aut Li-Ling, Jesse verfasserin aut Deng, Yihui verfasserin aut Enthalten in Journal of cancer research and clinical oncology Berlin : Springer, 1904 136(2009), 4 vom: 09. Okt., Seite 603-610 (DE-627)253769515 (DE-600)1459285-X 1432-1335 nnns volume:136 year:2009 number:4 day:09 month:10 pages:603-610 https://dx.doi.org/10.1007/s00432-009-0698-x 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_65 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_165 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_4328 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 136 2009 4 09 10 603-610 |
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10.1007/s00432-009-0698-x doi (DE-627)SPR005844525 (SPR)s00432-009-0698-x-e DE-627 ger DE-627 rakwb eng 610 ASE 44.81 bkl Sun, Chunyan verfasserin aut Inhibitory effect of cucurbitacin E on pancreatic cancer cells growth via STAT3 signaling 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Purpose Pancreatic cancer has been a serious disease worldwide for its high mortality. Cucurbitacin E is a member of triterpenoid family isolated from plants showing antiproliferative activity on various cancer cells. In this study, we have explored whether cucurbitacin E also has an anti-tumor effect on pancreatic cancer cells. Methods Human pancreatic cancer cells PANC-1 were used to explore the effect and possible mechanisms of cucurbitacin E on cell cycle progression, apoptosis and proliferation. Results Cucurbitacin E has inhibited the growth of PANC-1 cells in a dose- and time-dependent manner, and has caused accumulation of cells at the $ G_{2} $/M phase as well as apoptosis. Western blotting also showed that cucurbitacin E treatment can inhibit STAT3 phosphorylation while upregulate p53 expression. Conclusions Our results suggested that cucurbitacin E may be an effective regimen for the chemotherapy of pancreatic cancer. Cucurbitacin E (dpeaa)DE-He213 p53 (dpeaa)DE-He213 PANC-1 (dpeaa)DE-He213 Pancreatic cancer (dpeaa)DE-He213 STAT3 (dpeaa)DE-He213 Zhang, Meixia verfasserin aut Shan, Xiaolei verfasserin aut Zhou, Xueying verfasserin aut Yang, Jiao verfasserin aut Wang, Yanli verfasserin aut Li-Ling, Jesse verfasserin aut Deng, Yihui verfasserin aut Enthalten in Journal of cancer research and clinical oncology Berlin : Springer, 1904 136(2009), 4 vom: 09. Okt., Seite 603-610 (DE-627)253769515 (DE-600)1459285-X 1432-1335 nnns volume:136 year:2009 number:4 day:09 month:10 pages:603-610 https://dx.doi.org/10.1007/s00432-009-0698-x 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_65 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_165 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_4328 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 136 2009 4 09 10 603-610 |
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10.1007/s00432-009-0698-x doi (DE-627)SPR005844525 (SPR)s00432-009-0698-x-e DE-627 ger DE-627 rakwb eng 610 ASE 44.81 bkl Sun, Chunyan verfasserin aut Inhibitory effect of cucurbitacin E on pancreatic cancer cells growth via STAT3 signaling 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Purpose Pancreatic cancer has been a serious disease worldwide for its high mortality. Cucurbitacin E is a member of triterpenoid family isolated from plants showing antiproliferative activity on various cancer cells. In this study, we have explored whether cucurbitacin E also has an anti-tumor effect on pancreatic cancer cells. Methods Human pancreatic cancer cells PANC-1 were used to explore the effect and possible mechanisms of cucurbitacin E on cell cycle progression, apoptosis and proliferation. Results Cucurbitacin E has inhibited the growth of PANC-1 cells in a dose- and time-dependent manner, and has caused accumulation of cells at the $ G_{2} $/M phase as well as apoptosis. Western blotting also showed that cucurbitacin E treatment can inhibit STAT3 phosphorylation while upregulate p53 expression. Conclusions Our results suggested that cucurbitacin E may be an effective regimen for the chemotherapy of pancreatic cancer. Cucurbitacin E (dpeaa)DE-He213 p53 (dpeaa)DE-He213 PANC-1 (dpeaa)DE-He213 Pancreatic cancer (dpeaa)DE-He213 STAT3 (dpeaa)DE-He213 Zhang, Meixia verfasserin aut Shan, Xiaolei verfasserin aut Zhou, Xueying verfasserin aut Yang, Jiao verfasserin aut Wang, Yanli verfasserin aut Li-Ling, Jesse verfasserin aut Deng, Yihui verfasserin aut Enthalten in Journal of cancer research and clinical oncology Berlin : Springer, 1904 136(2009), 4 vom: 09. Okt., Seite 603-610 (DE-627)253769515 (DE-600)1459285-X 1432-1335 nnns volume:136 year:2009 number:4 day:09 month:10 pages:603-610 https://dx.doi.org/10.1007/s00432-009-0698-x 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_65 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_165 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_4328 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 136 2009 4 09 10 603-610 |
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10.1007/s00432-009-0698-x doi (DE-627)SPR005844525 (SPR)s00432-009-0698-x-e DE-627 ger DE-627 rakwb eng 610 ASE 44.81 bkl Sun, Chunyan verfasserin aut Inhibitory effect of cucurbitacin E on pancreatic cancer cells growth via STAT3 signaling 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Purpose Pancreatic cancer has been a serious disease worldwide for its high mortality. Cucurbitacin E is a member of triterpenoid family isolated from plants showing antiproliferative activity on various cancer cells. In this study, we have explored whether cucurbitacin E also has an anti-tumor effect on pancreatic cancer cells. Methods Human pancreatic cancer cells PANC-1 were used to explore the effect and possible mechanisms of cucurbitacin E on cell cycle progression, apoptosis and proliferation. Results Cucurbitacin E has inhibited the growth of PANC-1 cells in a dose- and time-dependent manner, and has caused accumulation of cells at the $ G_{2} $/M phase as well as apoptosis. Western blotting also showed that cucurbitacin E treatment can inhibit STAT3 phosphorylation while upregulate p53 expression. Conclusions Our results suggested that cucurbitacin E may be an effective regimen for the chemotherapy of pancreatic cancer. Cucurbitacin E (dpeaa)DE-He213 p53 (dpeaa)DE-He213 PANC-1 (dpeaa)DE-He213 Pancreatic cancer (dpeaa)DE-He213 STAT3 (dpeaa)DE-He213 Zhang, Meixia verfasserin aut Shan, Xiaolei verfasserin aut Zhou, Xueying verfasserin aut Yang, Jiao verfasserin aut Wang, Yanli verfasserin aut Li-Ling, Jesse verfasserin aut Deng, Yihui verfasserin aut Enthalten in Journal of cancer research and clinical oncology Berlin : Springer, 1904 136(2009), 4 vom: 09. Okt., Seite 603-610 (DE-627)253769515 (DE-600)1459285-X 1432-1335 nnns volume:136 year:2009 number:4 day:09 month:10 pages:603-610 https://dx.doi.org/10.1007/s00432-009-0698-x 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_65 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_165 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_4328 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 136 2009 4 09 10 603-610 |
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Enthalten in Journal of cancer research and clinical oncology 136(2009), 4 vom: 09. Okt., Seite 603-610 volume:136 year:2009 number:4 day:09 month:10 pages:603-610 |
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Sun, Chunyan @@aut@@ Zhang, Meixia @@aut@@ Shan, Xiaolei @@aut@@ Zhou, Xueying @@aut@@ Yang, Jiao @@aut@@ Wang, Yanli @@aut@@ Li-Ling, Jesse @@aut@@ Deng, Yihui @@aut@@ |
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<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">SPR005844525</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230519183552.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">201002s2009 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1007/s00432-009-0698-x</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)SPR005844525</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(SPR)s00432-009-0698-x-e</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">ASE</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">44.81</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Sun, Chunyan</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Inhibitory effect of cucurbitacin E on pancreatic cancer cells growth via STAT3 signaling</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2009</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Purpose Pancreatic cancer has been a serious disease worldwide for its high mortality. Cucurbitacin E is a member of triterpenoid family isolated from plants showing antiproliferative activity on various cancer cells. In this study, we have explored whether cucurbitacin E also has an anti-tumor effect on pancreatic cancer cells. Methods Human pancreatic cancer cells PANC-1 were used to explore the effect and possible mechanisms of cucurbitacin E on cell cycle progression, apoptosis and proliferation. Results Cucurbitacin E has inhibited the growth of PANC-1 cells in a dose- and time-dependent manner, and has caused accumulation of cells at the $ G_{2} $/M phase as well as apoptosis. Western blotting also showed that cucurbitacin E treatment can inhibit STAT3 phosphorylation while upregulate p53 expression. 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Sun, Chunyan |
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Sun, Chunyan ddc 610 bkl 44.81 misc Cucurbitacin E misc p53 misc PANC-1 misc Pancreatic cancer misc STAT3 Inhibitory effect of cucurbitacin E on pancreatic cancer cells growth via STAT3 signaling |
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610 ASE 44.81 bkl Inhibitory effect of cucurbitacin E on pancreatic cancer cells growth via STAT3 signaling Cucurbitacin E (dpeaa)DE-He213 p53 (dpeaa)DE-He213 PANC-1 (dpeaa)DE-He213 Pancreatic cancer (dpeaa)DE-He213 STAT3 (dpeaa)DE-He213 |
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ddc 610 bkl 44.81 misc Cucurbitacin E misc p53 misc PANC-1 misc Pancreatic cancer misc STAT3 |
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Inhibitory effect of cucurbitacin E on pancreatic cancer cells growth via STAT3 signaling |
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inhibitory effect of cucurbitacin e on pancreatic cancer cells growth via stat3 signaling |
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Inhibitory effect of cucurbitacin E on pancreatic cancer cells growth via STAT3 signaling |
| abstract |
Purpose Pancreatic cancer has been a serious disease worldwide for its high mortality. Cucurbitacin E is a member of triterpenoid family isolated from plants showing antiproliferative activity on various cancer cells. In this study, we have explored whether cucurbitacin E also has an anti-tumor effect on pancreatic cancer cells. Methods Human pancreatic cancer cells PANC-1 were used to explore the effect and possible mechanisms of cucurbitacin E on cell cycle progression, apoptosis and proliferation. Results Cucurbitacin E has inhibited the growth of PANC-1 cells in a dose- and time-dependent manner, and has caused accumulation of cells at the $ G_{2} $/M phase as well as apoptosis. Western blotting also showed that cucurbitacin E treatment can inhibit STAT3 phosphorylation while upregulate p53 expression. Conclusions Our results suggested that cucurbitacin E may be an effective regimen for the chemotherapy of pancreatic cancer. |
| abstractGer |
Purpose Pancreatic cancer has been a serious disease worldwide for its high mortality. Cucurbitacin E is a member of triterpenoid family isolated from plants showing antiproliferative activity on various cancer cells. In this study, we have explored whether cucurbitacin E also has an anti-tumor effect on pancreatic cancer cells. Methods Human pancreatic cancer cells PANC-1 were used to explore the effect and possible mechanisms of cucurbitacin E on cell cycle progression, apoptosis and proliferation. Results Cucurbitacin E has inhibited the growth of PANC-1 cells in a dose- and time-dependent manner, and has caused accumulation of cells at the $ G_{2} $/M phase as well as apoptosis. Western blotting also showed that cucurbitacin E treatment can inhibit STAT3 phosphorylation while upregulate p53 expression. Conclusions Our results suggested that cucurbitacin E may be an effective regimen for the chemotherapy of pancreatic cancer. |
| abstract_unstemmed |
Purpose Pancreatic cancer has been a serious disease worldwide for its high mortality. Cucurbitacin E is a member of triterpenoid family isolated from plants showing antiproliferative activity on various cancer cells. In this study, we have explored whether cucurbitacin E also has an anti-tumor effect on pancreatic cancer cells. Methods Human pancreatic cancer cells PANC-1 were used to explore the effect and possible mechanisms of cucurbitacin E on cell cycle progression, apoptosis and proliferation. Results Cucurbitacin E has inhibited the growth of PANC-1 cells in a dose- and time-dependent manner, and has caused accumulation of cells at the $ G_{2} $/M phase as well as apoptosis. Western blotting also showed that cucurbitacin E treatment can inhibit STAT3 phosphorylation while upregulate p53 expression. Conclusions Our results suggested that cucurbitacin E may be an effective regimen for the chemotherapy of pancreatic cancer. |
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| score |
7.401602 |