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Nuclear Factor-κB Dimer Exchange Promotes a p21waf1/cip1 Superinduction Response in Human T Leukemic Cells
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| Zeitschriftentitel: | Molecular Cancer Research |
|---|---|
| Personen und Körperschaften: | , |
| In: | Molecular Cancer Research, 4, 2006, 2, S. 101-112 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
American Association for Cancer Research (AACR)
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| Schlagwörter: |
| author_facet |
Chang, Pei-Yun Miyamoto, Shigeki Chang, Pei-Yun Miyamoto, Shigeki |
|---|---|
| author |
Chang, Pei-Yun Miyamoto, Shigeki |
| spellingShingle |
Chang, Pei-Yun Miyamoto, Shigeki Molecular Cancer Research Nuclear Factor-κB Dimer Exchange Promotes a p21waf1/cip1 Superinduction Response in Human T Leukemic Cells Cancer Research Oncology Molecular Biology |
| author_sort |
chang, pei-yun |
| spelling |
Chang, Pei-Yun Miyamoto, Shigeki 1541-7786 1557-3125 American Association for Cancer Research (AACR) Cancer Research Oncology Molecular Biology http://dx.doi.org/10.1158/1541-7786.mcr-05-0259 <jats:title>Abstract</jats:title><jats:p>The nuclear factor-κB (NF-κB)/Rel transcription factors are recognized as critical apoptosis regulators. We reported previously that NF-κB contributes to chemoresistance of CEM human T leukemic cells in part through its ability to induce p21waf1/cip1. Here, we provide evidence that sequential NF-κB-activating signals induce heightened NF-κB DNA binding and p21waf1/cip1 induction in CEM and additional T leukemic cell lines. This response arises from exceedingly low basal expression of the p105/p50 NF-κB subunit encoded by the NFKB1 gene in these cell lines. An initial NF-κB activation event enhances the recruitment of p65 and ELF1 to the NFKB1 promoter, leading to p65- and ELF1-dependent synthesis of p105/p50, which promotes an exchange of NF-κB complexes to p50-containing complexes with an increased DNA-binding activity to certain NF-κB target elements. Subsequent stimulation of these cells with an anticancer agent, etoposide, results in augmented NF-κB-dependent p21waf1/cip1 induction and increased chemoresistance of the leukemia cells. Thus, we propose that low basal NFKB1 expression coupled with sequential NF-κB activation events can promote increased chemoresistance in certain T leukemic cells. (Mol Cancer Res 2006;4(2):101–12)</jats:p> Nuclear Factor-κB Dimer Exchange Promotes a p21waf1/cip1 Superinduction Response in Human T Leukemic Cells Molecular Cancer Research |
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American Association for Cancer Research (AACR), 2006 |
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| title |
Nuclear Factor-κB Dimer Exchange Promotes a p21waf1/cip1 Superinduction Response in Human T Leukemic Cells |
| title_unstemmed |
Nuclear Factor-κB Dimer Exchange Promotes a p21waf1/cip1 Superinduction Response in Human T Leukemic Cells |
| title_full |
Nuclear Factor-κB Dimer Exchange Promotes a p21waf1/cip1 Superinduction Response in Human T Leukemic Cells |
| title_fullStr |
Nuclear Factor-κB Dimer Exchange Promotes a p21waf1/cip1 Superinduction Response in Human T Leukemic Cells |
| title_full_unstemmed |
Nuclear Factor-κB Dimer Exchange Promotes a p21waf1/cip1 Superinduction Response in Human T Leukemic Cells |
| title_short |
Nuclear Factor-κB Dimer Exchange Promotes a p21waf1/cip1 Superinduction Response in Human T Leukemic Cells |
| title_sort |
nuclear factor-κb dimer exchange promotes a p21waf1/cip1 superinduction response in human t leukemic cells |
| topic |
Cancer Research Oncology Molecular Biology |
| url |
http://dx.doi.org/10.1158/1541-7786.mcr-05-0259 |
| publishDate |
2006 |
| physical |
101-112 |
| description |
<jats:title>Abstract</jats:title><jats:p>The nuclear factor-κB (NF-κB)/Rel transcription factors are recognized as critical apoptosis regulators. We reported previously that NF-κB contributes to chemoresistance of CEM human T leukemic cells in part through its ability to induce p21waf1/cip1. Here, we provide evidence that sequential NF-κB-activating signals induce heightened NF-κB DNA binding and p21waf1/cip1 induction in CEM and additional T leukemic cell lines. This response arises from exceedingly low basal expression of the p105/p50 NF-κB subunit encoded by the NFKB1 gene in these cell lines. An initial NF-κB activation event enhances the recruitment of p65 and ELF1 to the NFKB1 promoter, leading to p65- and ELF1-dependent synthesis of p105/p50, which promotes an exchange of NF-κB complexes to p50-containing complexes with an increased DNA-binding activity to certain NF-κB target elements. Subsequent stimulation of these cells with an anticancer agent, etoposide, results in augmented NF-κB-dependent p21waf1/cip1 induction and increased chemoresistance of the leukemia cells. Thus, we propose that low basal NFKB1 expression coupled with sequential NF-κB activation events can promote increased chemoresistance in certain T leukemic cells. (Mol Cancer Res 2006;4(2):101–12)</jats:p> |
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| author | Chang, Pei-Yun, Miyamoto, Shigeki |
| author_facet | Chang, Pei-Yun, Miyamoto, Shigeki, Chang, Pei-Yun, Miyamoto, Shigeki |
| author_sort | chang, pei-yun |
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| description | <jats:title>Abstract</jats:title><jats:p>The nuclear factor-κB (NF-κB)/Rel transcription factors are recognized as critical apoptosis regulators. We reported previously that NF-κB contributes to chemoresistance of CEM human T leukemic cells in part through its ability to induce p21waf1/cip1. Here, we provide evidence that sequential NF-κB-activating signals induce heightened NF-κB DNA binding and p21waf1/cip1 induction in CEM and additional T leukemic cell lines. This response arises from exceedingly low basal expression of the p105/p50 NF-κB subunit encoded by the NFKB1 gene in these cell lines. An initial NF-κB activation event enhances the recruitment of p65 and ELF1 to the NFKB1 promoter, leading to p65- and ELF1-dependent synthesis of p105/p50, which promotes an exchange of NF-κB complexes to p50-containing complexes with an increased DNA-binding activity to certain NF-κB target elements. Subsequent stimulation of these cells with an anticancer agent, etoposide, results in augmented NF-κB-dependent p21waf1/cip1 induction and increased chemoresistance of the leukemia cells. Thus, we propose that low basal NFKB1 expression coupled with sequential NF-κB activation events can promote increased chemoresistance in certain T leukemic cells. (Mol Cancer Res 2006;4(2):101–12)</jats:p> |
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| imprint_str_mv | American Association for Cancer Research (AACR), 2006 |
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| spelling | Chang, Pei-Yun Miyamoto, Shigeki 1541-7786 1557-3125 American Association for Cancer Research (AACR) Cancer Research Oncology Molecular Biology http://dx.doi.org/10.1158/1541-7786.mcr-05-0259 <jats:title>Abstract</jats:title><jats:p>The nuclear factor-κB (NF-κB)/Rel transcription factors are recognized as critical apoptosis regulators. We reported previously that NF-κB contributes to chemoresistance of CEM human T leukemic cells in part through its ability to induce p21waf1/cip1. Here, we provide evidence that sequential NF-κB-activating signals induce heightened NF-κB DNA binding and p21waf1/cip1 induction in CEM and additional T leukemic cell lines. This response arises from exceedingly low basal expression of the p105/p50 NF-κB subunit encoded by the NFKB1 gene in these cell lines. An initial NF-κB activation event enhances the recruitment of p65 and ELF1 to the NFKB1 promoter, leading to p65- and ELF1-dependent synthesis of p105/p50, which promotes an exchange of NF-κB complexes to p50-containing complexes with an increased DNA-binding activity to certain NF-κB target elements. Subsequent stimulation of these cells with an anticancer agent, etoposide, results in augmented NF-κB-dependent p21waf1/cip1 induction and increased chemoresistance of the leukemia cells. Thus, we propose that low basal NFKB1 expression coupled with sequential NF-κB activation events can promote increased chemoresistance in certain T leukemic cells. (Mol Cancer Res 2006;4(2):101–12)</jats:p> Nuclear Factor-κB Dimer Exchange Promotes a p21waf1/cip1 Superinduction Response in Human T Leukemic Cells Molecular Cancer Research |
| spellingShingle | Chang, Pei-Yun, Miyamoto, Shigeki, Molecular Cancer Research, Nuclear Factor-κB Dimer Exchange Promotes a p21waf1/cip1 Superinduction Response in Human T Leukemic Cells, Cancer Research, Oncology, Molecular Biology |
| title | Nuclear Factor-κB Dimer Exchange Promotes a p21waf1/cip1 Superinduction Response in Human T Leukemic Cells |
| title_full | Nuclear Factor-κB Dimer Exchange Promotes a p21waf1/cip1 Superinduction Response in Human T Leukemic Cells |
| title_fullStr | Nuclear Factor-κB Dimer Exchange Promotes a p21waf1/cip1 Superinduction Response in Human T Leukemic Cells |
| title_full_unstemmed | Nuclear Factor-κB Dimer Exchange Promotes a p21waf1/cip1 Superinduction Response in Human T Leukemic Cells |
| title_short | Nuclear Factor-κB Dimer Exchange Promotes a p21waf1/cip1 Superinduction Response in Human T Leukemic Cells |
| title_sort | nuclear factor-κb dimer exchange promotes a p21waf1/cip1 superinduction response in human t leukemic cells |
| title_unstemmed | Nuclear Factor-κB Dimer Exchange Promotes a p21waf1/cip1 Superinduction Response in Human T Leukemic Cells |
| topic | Cancer Research, Oncology, Molecular Biology |
| url | http://dx.doi.org/10.1158/1541-7786.mcr-05-0259 |