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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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| Authors: | Antonietta R. Farina Lucia Cappabianca Pierdomenico RuggeriNatalia Di Ianni Marzia RagoneStefania Merolle Kimihiko SanoMary L. Stracke Jonathan M. HorowitzAlberto Gulino Andrew R. Mackay |
| Affiliation: | a Section of Molecular Pathology, Department of Experimental Medicine, University of L’Aquila, 67100 L’Aquila, Italy b Department of Pediatrics, Kobe University School of Medicine, Kobe 650, Japan c Laboratory of Pathology, NCI, NIH, Bethesda, MD 20892, USA d Department of Anatomy, Physiological Sciences and Radiology, North Carolina State University, Raleigh, NC 27606, USA e Department of Experimental Medicine and Pathology, University of Rome “La Sapienza”, 00161 Rome, Italy |
| Abstract: | 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. |
| Keywords: | 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, activator protein-1 SP, specificity protein |
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