Nuclear localisation of nuclear factor-kappaB transcription factors in prostate cancer: an immunohistochemical study.
Nuclear localisation of nuclear factor-kappaB transcription factors in prostate cancer: an immunohistochemical study.
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DOI：
10.1038/sj.bjc.6602796
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发表时间：
2005-10-31
影响因子：
8.8
通讯作者：
中科院分区：
文献类型：
--
作者：
一些报告表明，典型的核因子-κ B（NF-κB）途径在前列腺癌细胞亚群中被组成性激活。然而，除了RelA（p65），关于NF-κB转录因子在前列腺癌组织中的状态知之甚少。为了阐明NF-κB亚单位的状态，我们分析了RelA、RelB、c-Rel、p50和p52在75例患者的组织阵列切片上的表达和亚细胞定位，组织阵列切片分别包含344、346、369、343和344个核心。根据相关临床参数（术前前列腺特异性抗原、病理分期和术后Gleason分级）检测NF-κB因子的亚细胞定位。除c-Rel外，每个亚基均在癌细胞核中检测到：RelB、RelA、p52和p50的显著核表达分别见于26.6%、15.6%、10.7%和10.5%的核心。令人惊讶的是，表达核RelA和p50经典途径蛋白的核心比表达其他亚基组合（例如RelB-p52和RelA-RelB）的核心不太常见。此外，RelB的核定位与患者的Gleason评分相关（斯皮尔曼相关性：0.167; P=0.018）。经典和非经典NF-κB亚基在前列腺癌细胞中的核定位首次表明，不同的NF-κB途径和二聚体可能在疾病的进展中被激活。
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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