Downregulation of nuclear factor-[kappa]B p65 subunit by small interfering RNA synergizes with gemcitabine to inhibit the growth of pancreatic cancer
The clinical benefit of gemcitabine for pancreatic cancer is low due to chemoresistance. Nuclear factor (NF)-κB, constitutively activated in pancreatic cancer, is a therapeutic target as it upregulates expression of genes controlling proliferation, apoptosis and angiogenesis. This study aimed to inv...
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| Veröffentlicht in: | Cancer letters 2010-05, Vol.291 (1), p.90 |
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| container_title | Cancer letters |
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| creator | Kong, Rui Sun, Bei Jiang, Hongchi Pan, Shangha Chen, Hua Wang, Shuangjia Krissansen, Geoffrey W Sun, Xueying |
| description | The clinical benefit of gemcitabine for pancreatic cancer is low due to chemoresistance. Nuclear factor (NF)-κB, constitutively activated in pancreatic cancer, is a therapeutic target as it upregulates expression of genes controlling proliferation, apoptosis and angiogenesis. This study aimed to investigate whether downregulation of the p65 subunit of NF-κB by siRNA could enhance the efficacy of gemcitabine to treat pancreatic cancer. p65 siRNA synergized with gemcitabine to inhibit the proliferation and induce the apoptosis of pancreatic cancer cellsin vitroandin vivo, and suppress the growth and angiogenesis of pancreatic tumors in nude mice. The mechanisms involved inhibition of NF-κB activity and consequent inhibition of Bcl-2, cyclin D1 and VEGF, and activation of caspase-3. The results suggest that downregulation of NF-κB p65 potentiates the efficacy of gemcitabine in combating pancreatic cancer. |
| doi_str_mv | 10.1016/j.canlet.2009.10.001 |
| format | Article |
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Nuclear factor (NF)-κB, constitutively activated in pancreatic cancer, is a therapeutic target as it upregulates expression of genes controlling proliferation, apoptosis and angiogenesis. This study aimed to investigate whether downregulation of the p65 subunit of NF-κB by siRNA could enhance the efficacy of gemcitabine to treat pancreatic cancer. p65 siRNA synergized with gemcitabine to inhibit the proliferation and induce the apoptosis of pancreatic cancer cellsin vitroandin vivo, and suppress the growth and angiogenesis of pancreatic tumors in nude mice. The mechanisms involved inhibition of NF-κB activity and consequent inhibition of Bcl-2, cyclin D1 and VEGF, and activation of caspase-3. 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Nuclear factor (NF)-κB, constitutively activated in pancreatic cancer, is a therapeutic target as it upregulates expression of genes controlling proliferation, apoptosis and angiogenesis. This study aimed to investigate whether downregulation of the p65 subunit of NF-κB by siRNA could enhance the efficacy of gemcitabine to treat pancreatic cancer. p65 siRNA synergized with gemcitabine to inhibit the proliferation and induce the apoptosis of pancreatic cancer cellsin vitroandin vivo, and suppress the growth and angiogenesis of pancreatic tumors in nude mice. The mechanisms involved inhibition of NF-κB activity and consequent inhibition of Bcl-2, cyclin D1 and VEGF, and activation of caspase-3. 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| fulltext | fulltext |
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| ispartof | Cancer letters, 2010-05, Vol.291 (1), p.90 |
| issn | 0304-3835 1872-7980 |
| language | eng |
| recordid | cdi_proquest_journals_1550185726 |
| source | Elsevier ScienceDirect Journals |
| subjects | Angiogenesis Apoptosis Cancer therapies Cell cycle Cytotoxicity Pancreas Pancreatic cancer Studies Tumors Vascular endothelial growth factor |
| title | Downregulation of nuclear factor-[kappa]B p65 subunit by small interfering RNA synergizes with gemcitabine to inhibit the growth of pancreatic cancer |
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