Section of Molecular Pathology, Department of Experimental Medicine, University of L'Aquila, 67100 L'Aquila, Italy.
FEBS Lett. 2012 Oct 19;586(20):3681-91. doi: 10.1016/j.febslet.2012.08.026. Epub 2012 Sep 6.
The motility, angiogenesis and metastasis-stimulating factor Autotaxin (Atx), over expressed by human neuroblastomas (NB), is constitutively expressed by human Nmyc-amplified SK-N-BE and non-Nmyc-amplified SH-SY5Y NB cells. Here, we characterise a novel Atx transcriptional mechanism, utilised by both cell lines, that is restricted to the first 285bp of the Atx promoter and involves AP-1 and SP transcription factors, acting through a CRE/AP-1-like element at position -142 to -149 and a GAbox at position -227 to -235 relative to the Atx translational start site. This novel transcriptional mechanism can be inhibited by internally initiated SP-3 and the natural phenol curcumin.
神经母细胞瘤（NB）过表达的运动、血管生成和转移刺激因子自分泌酶（Atx）在人类 Nmyc 扩增的 SK-N-BE 和非 Nmyc 扩增的 SH-SY5Y NB 细胞中组成性表达。在这里，我们描述了一种新的 Atx 转录机制，该机制被两种细胞系利用，仅限于 Atx 启动子的前 285bp，涉及 AP-1 和 SP 转录因子，通过位于 Atx 翻译起始位点的-142 到-149 处的 CRE/AP-1 样元件和-227 到-235 处的 GAbox 发挥作用。这种新的转录机制可以被内部起始的 SP-3 和天然酚类姜黄素抑制。
