Wang Jian, Chen Guohua, Pantopoulos Kostas
Lady Davis Institute for Medical Research, Sir Mortimer B. Davis Jewish General Hospital, 3755 Cote-Ste-Catherine Road, Montreal, Quebec, Canada H3T 1E2.
Biochem J. 2005 Dec 1;392(Pt 2):383-8. doi: 10.1042/BJ20050492.
TfR1 (transferrin receptor 1) mediates the uptake of transferrin-bound iron and thereby plays a critical role in cellular iron metabolism. Its expression is coupled to cell proliferation/differentiation and controlled in response to iron levels and other signals by transcriptional and post-transcriptional mechanisms. It is well established that TfR1 levels decline when cultured cells reach a high density and in the present study we have investigated the underlying mechanisms. Consistent with previous findings, we demonstrate that TfR1 expression is attenuated in a cell-density-dependent manner in human lung cancer H1299 cells and in murine B6 fibroblasts as the result of a marked decrease in mRNA content. This response is not associated with alterations in the RNA-binding activity of iron regulatory proteins that are indicative of a transcriptional mechanism. Reporter assays reveal that the human TfR1 promoters contains sequences mediating cell-density-dependent transcriptional inhibition. Mapping of the human and mouse TfR1 promoters identified a conserved hexa-nucleotide 5'-GAGGGC-3' motif with notable sequence similarity to a previously described element within the IGF-2 (insulin-like growth factor-2) promoter. We show that this motif is necessary for the formation of specific complexes with nuclear extracts and for cell-density-dependent regulation in reporter gene assays. Thus the TfR1 promoter contains a functional 'cell density response element' (CDRE).
转铁蛋白受体1(TfR1)介导结合转铁蛋白的铁的摄取,因此在细胞铁代谢中起关键作用。其表达与细胞增殖/分化相关联,并通过转录和转录后机制响应铁水平及其他信号而受到调控。众所周知,当培养细胞达到高密度时,TfR1水平会下降,在本研究中我们探究了其潜在机制。与先前的研究结果一致,我们证明在人肺癌H1299细胞和小鼠B6成纤维细胞中,TfR1表达以细胞密度依赖性方式减弱,这是mRNA含量显著降低的结果。这种反应与铁调节蛋白的RNA结合活性改变无关,而铁调节蛋白的RNA结合活性改变是转录机制的指示。报告基因检测显示,人TfR1启动子包含介导细胞密度依赖性转录抑制的序列。对人和小鼠TfR1启动子的定位鉴定出一个保守的六核苷酸5'-GAGGGC-3'基序,其与胰岛素样生长因子-2(IGF-2)启动子内先前描述的元件具有显著的序列相似性。我们表明,该基序对于与核提取物形成特异性复合物以及在报告基因检测中进行细胞密度依赖性调节是必需的。因此,TfR1启动子包含一个功能性的“细胞密度反应元件”(CDRE)。