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Nuclear localisation of nuclear factor-kappaB transcription factors in prostate cancer: an immunohistochemical study
Several reports suggest that the canonical nuclear factor-kappaB (NF-κB) pathway is constitutively activated in a subset of prostate cancer cells. However, except for RelA (p65), little is known about the status of NF-κB transcription factors in prostate cancer tissues. To clarify the status of NF-κ...
Autores principales: | , , , , |
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Formato: | Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group
2005
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2361687/ https://www.ncbi.nlm.nih.gov/pubmed/16205698 http://dx.doi.org/10.1038/sj.bjc.6602796 |
Sumario: | Several reports suggest that the canonical nuclear factor-kappaB (NF-κB) pathway is constitutively activated in a subset of prostate cancer cells. However, except for RelA (p65), little is known about the status of NF-κB transcription factors in prostate cancer tissues. To clarify the status of NF-κB subunits, we analysed the expression and subcellular localisation of RelA, RelB, c-Rel, p50, and p52 on tissue array sections containing respectively 344, 346, 369, 343, and 344 cores from 75 patients. The subcellular localisation of NF-κB factors was tested against relevant clinical parameters (preoperative prostate-specific antigen, pathological stage, and postoperative Gleason grade). With the exception of c-Rel, each subunit was detected in the nucleus of cancer cells: significant nuclear expression of RelB, RelA, p52, and p50 was seen in 26.6, 15.6, 10.7, and 10.5% of cores, respectively. Surprisingly, cores expressing both nuclear RelA and p50 canonical pathway proteins were less frequently observed than cores expressing other subunit combinations such as RelB–p52 and RelA–RelB. In addition, the nuclear localisation of RelB correlated with patient's Gleason scores (Spearman correlation: 0.167; P=0.018). The nuclear localisation of both canonical and noncanonical NF-κB subunits in prostate cancer cells suggests for the first time that different NF-κB pathways and dimers may be activated in the progression of the disease. |
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