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Vitamin D-induced up-regulation of tumour necrosis factor alpha (TNF-alpha) in prostate cancer cells

机译：维生素D诱导前列腺癌细胞肿瘤坏死因子α（TNF-alpha）的上调

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摘要

1 alpha,25-dihydroxyvitamin D3 (1 alpha,25(OH)(2)D-3 or calcitriol) is an active hormone that regulates cellular proliferation and induces apoptosis in cancer cells. Here we report on a new calcitriol target gene in prostate cancer cells, tumour necrosis factor alpha (TNF-alpha). Calcitriol and its analogue CB1093 up regulate TNF-alpha mRNA expression in LNCaP and PC-3 cells. The stimulation is dose-dependent in both of these cell lines, demonstrated by the quantitative real-time polyrnerase chain reaction. Calcitriol and CB1093 act synergistically with human recombinant TNF-alpha in activation of TNF-alpha mRNA expression in LNCaP but not in PC 3 cells. Transcriptional activation of TNF-alpha gene by calcitriol or CB1093 does not lead to TNF-alpha protein secretion, however calcitriol and CB1093 enhance TPA-stimulated TNF-alpha production in LNCaP cells. We did not observe any significant effect of calcitriol on regulation of TNFR1 at the level of gene expression, Nor does calcitriol affect transcriptional regulation of cytokine (IL-1, LL-6) and cytokine receptor genes in LNCaP and PC -3 prostate cancer cell lines. Calcitriol and its analogue CB1093 at 10 nM concentration induce programmed cell death in LNCaP` cells, Combined addition of human recombinant TN F-alpha with calcitriol or CB1093 cause enhanced effect in induction of apoptosis. We conclude that under physiological conditions vitamin D activates only the transcription of TNF-alpha gene, for TNF-alpha protein synthesis additional cofactors are required, Therefore a cooperation of vitamin D and TNF-alpha may play an important role in the control of cell growth in prostate cancer. (c) 2005 Elsevier Inc. All rights reserved.
机译：1α，25-二羟基维生素D3（1α，25（OH）（2）D-3或骨化三醇）是一种活性激素，可调节细胞增殖并诱导癌细胞凋亡。在这里，我们报道前列腺癌细胞中的新骨化三​​醇靶基因，肿瘤坏死因子α（TNF-α）。骨化三醇及其类似物CB1093上调LNCaP和PC-3细胞中的TNF-αmRNA表达。在这两种细胞系中，刺激都是剂量依赖性的，这通过定量实时聚合酶链反应得以证明。骨化三醇和CB1093与人重组TNF-α协同作用，激活LNCaP中的TNF-αmRNA表达，但不激活PC 3细胞。骨化三醇或CB1093转录激活TNF-α基因不会导致TNF-α蛋白分泌，但是骨化三醇和CB1093增强LNCaP细胞中TPA刺激的TNF-α产生。我们没有观察到骨化三醇在基因表达水平上对TNFR1调节的任何显着影响，也没有骨化三醇影响LNCaP和PC -3前列腺癌细胞中细胞因子（IL-1，LL-6）和细胞因子受体基因的转录调节线。骨化三醇及其类似物CB1093在10 nM的浓度下会诱导LNCaP`细胞中程序性细胞死亡，将人重组TNF-α与骨化三醇或CB1093联合添加可增强诱导细胞凋亡的作用。我们得出的结论是，在生理条件下，维生素D仅激活TNF-α基因的转录，对于TNF-α蛋白合成，还需要其他辅因子，因此，维生素D和TNF-α的协同作用可能在控制细胞生长中起重要作用在前列腺癌中。 （c）2005 Elsevier Inc.保留所有权利。

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