Department of Pathology, The University of Chicago, Chicago, IL 60637, USA.
Gene. 2010 May 15;456(1-2):36-44. doi: 10.1016/j.gene.2010.02.008. Epub 2010 Mar 3.
NOL7 is a candidate tumor suppressor gene that localizes to 6p23, a chromosomal region frequently associated with loss of heterozygosity in a number of malignancies including cervical cancer (CC). Re-expression of NOL7 in CC cells suppresses in vivo tumor growth by 95% and alters the angiogenic phenotype by modulating the expression of VEGF and TSP1. Here, we describe the determination of two NOL7 transcriptional start sites (TSS), the cloning of its regulatory promoter region, and the identification of transcription factors that regulate its expression. Using 5' Rapid amplification of complementary DNA ends (RACE), two transcriptional start sites were identified. Deletion analysis determined that the essential elements required for the optimal promoter activity of NOL7 were 560 bp upstream of its translation start site. In silico analysis suggested that the promoter region contained potential binding sites for the SP1, c-Myc and RXRalpha transcription factors as well as an overall GC content of greater than 60%. Chromatin immunoprecipitation (ChIP) confirmed that SP1, c-Myc and RXRalpha bound to the NOL7 promoter region. Finally, we demonstrate that NOL7 expression was positively regulated by c-Myc and RXRalpha. These results demonstrate that the NOL7 promoter region possesses each of the key elements of a TATA-less promoter. In addition, the positive regulation of NOL7 by c-Myc and RXRalpha provides additional mechanistic insights into the potential role of NOL7 in CC and other malignancies.
NOL7 是一个候选肿瘤抑制基因,定位于 6p23,该染色体区域常与多种恶性肿瘤(包括宫颈癌)的杂合性丢失有关。在宫颈癌细胞中重新表达 NOL7,可使体内肿瘤生长抑制 95%,并通过调节 VEGF 和 TSP1 的表达改变血管生成表型。在这里,我们描述了确定 NOL7 的两个转录起始位点(TSS)、克隆其调控启动子区以及鉴定调节其表达的转录因子的方法。使用 5' 快速扩增互补 DNA 末端(RACE),鉴定出两个转录起始位点。缺失分析确定,NOL7 最佳启动子活性所需的必需元件位于其翻译起始位点上游 560bp 处。计算机分析表明,该启动子区域包含潜在的 SP1、c-Myc 和 RXRalpha 转录因子结合位点,以及整体 GC 含量大于 60%。染色质免疫沉淀(ChIP)证实 SP1、c-Myc 和 RXRalpha 与 NOL7 启动子区域结合。最后,我们证明 NOL7 的表达受 c-Myc 和 RXRalpha 的正向调控。这些结果表明,NOL7 启动子区域具有 TATA -less 启动子的所有关键元件。此外,c-Myc 和 RXRalpha 对 NOL7 的正向调控为 NOL7 在宫颈癌和其他恶性肿瘤中的潜在作用提供了额外的机制见解。