Constitutive autotaxin transcription by Nmyc-amplified and non-amplified neuroblastoma cells is regulated by a novel AP-1 and SP-mediated mechanism and abrogated by curcumin
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- 作者：Antonietta R. Farina ; Lucia Cappabianca ; Pierdomenico Ruggeri ; Natalia Di Ianni ; Marzia Ragone ; Stefania Merolle ; Kimihiko Sano ; Mary L. Stracke ; Jonathan M. Horowitz ; Alberto Gulino ; Andrew R. Mackay
- 关键词：Atx ; autotaxin ; NB ; neuroblastoma ; CRE ; cAMP response element ; CREB ; CRE binding protein ; ATF ; activating transcription factor ; GAPDH ; glyceraldehyde-3-phosphate dehydrogenase ; EMSA ; electro-mobility shift assay ; ChIp ; chromatin immunoprecipitation ; AP1
- 刊名：FEBS Letters
- 出版年：2012
- 出版时间：19 October, 2012
- 年：2012
- 卷：586
- 期：20
- 页码：3681-3691
- 全文大小：900 K
文摘
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 285 bp 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.