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  • 1.
    Persson, Paula
    et al.
    Department of Laboratory Medicine, Lund University, University Hospital MAS, Malmö, Sweden.
    Manetopoulos, Christina
    Department of Laboratory Medicine, Lund University, University Hospital MAS, Malmö, Sweden.
    Lagergren, Anna
    Department for Stem Cell Biology, Lund University, Lund, Sweden.
    Nygren, Jens Martin
    Department for Stem Cell Biology, Lund University, Lund, Sweden.
    Gisler, Ramiro
    Department for Stem Cell Biology, Lund University, Lund, Sweden.
    Axelson, Håkan
    Department of Laboratory Medicine, Lund University, University Hospital MAS, Malmö, Sweden.
    Sigvardsson, Mikael
    Department for Stem Cell Biology, Lund University, Lund, Sweden.
    Olf/EBF proteins are expressed in neuroblastoma cells: potential regulators of the Chromogranin A and SCG10 promoters2004In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 110, no 1, p. 22-30Article in journal (Refereed)
    Abstract [en]

    The childhood malignancy neuroblastoma is derived from developmentally arrested sympathetic nervous system precursor cells. To obtain further insight into the molecular processes involved in the formation of these tumors, we decided to investigate the functional role of Olf/EBF (O/E) transcription factors in human neuroblastoma cells. We here report that O/E-1 and O/E-2 are expressed at variable levels in neuroblastoma cell lines and that O/E proteins could be identified by electrophoretic mobility shift assays. To identify potential neuronal target genes for O/E proteins in neuroblastoma cells we investigated the ability of a set of neuronal promoters to interact with O/E-1 in electrophoretic mobility shift assays. This analysis suggested that the Chromogranin A (CgA) and SCG10 promoters both contained binding sites for O/E-1. O/E-1 was able to activate the CgA promoter in vivo and mutation of the O/E-1 binding site in the CgA promoter reduced the functional activity of the element to about 60% of the wild-type in neuroblastoma cells, supporting the idea that O/E proteins may be involved in the control of the CgA promoter. Furthermore, overexpression of O/E-1 in hippocampal progenitor cells led to neurite outgrowth, indicative of a role for O/E proteins in neuronal differentiation.

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