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Retinoic acid–induced expression of autotaxin in N‐ myc –amplified neuroblastoma cells
Author(s) -
DufnerBeattie J.,
Lemons R. S.,
Thorburn A.
Publication year - 2001
Publication title -
molecular carcinogenesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.254
H-Index - 97
eISSN - 1098-2744
pISSN - 0899-1987
DOI - 10.1002/mc.1028
Subject(s) - biology , neuroblastoma , retinoic acid , autotaxin , retinoic acid receptor , cancer research , retinoic acid receptor gamma , lysophosphatidic acid , transcription factor , microbiology and biotechnology , autocrine signalling , gene expression , tretinoin , gene , cell culture , receptor , biochemistry , genetics
Neuroblastoma, the most common extracranial solid tumor in children, arises from precursors of the sympathetic nervous system. Neuroblastoma cell lines are responsive to the differentiation agent retinoic acid, which induces its effects by altering transcription rates of specific target genes. We identified autotaxin ( ATX ), which encodes an autocrine tumor motility‐stimulating factor, as a gene whose expression is significantly induced by retinoic acid in neuroblastoma cells. ATX induction was specific for neuroblastoma cell lines that contain N‐ myc amplification, a cytogenetic feature commonly associated with aggressive neuroblastomas. Although ATX expression was associated with amplification of the N‐ myc locus, N‐myc itself was neither sufficient nor required for ATX expression, suggesting that a coamplified gene is responsible. ATX induction by retinoic acid was due to increased transcription and required new protein synthesis. © 2001 Wiley‐Liss, Inc.