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  • Title: Overexpression of NM23-1 enhances responsiveness of IMR-32 human neuroblastoma cells to differentiation stimuli.
    Author: Backer MV, Kamel N, Sandoval C, Jayabose S, Mendola CE, Backer JM.
    Journal: Anticancer Res; 2000; 20(3A):1743-9. PubMed ID: 10928103.
    Abstract:
    BACKGROUND: Aggressiveness of neuroblastoma is associated with increased expression of the putative metastasis suppressor genes, nm23-1 and nm23-2. These genes encode nucleoside diphosphate kinases A and B that form free or bound homo- and heteromers, which are distributed between soluble and particulate fractions of cells and display catalytic and non-catalytic activities. MATERIALS AND METHODS: In order to establish which forms and activities of nm23 proteins are operative in neuroblastoma we stably transfected IMR-32 human neuroblastoma cells with constructs encoding wild type and catalytically inactive nm23-1 and nm23-2 proteins. RESULTS: Overexpression of wild type nm23-1 proteins stimulated spontaneous neurite outgrowth and enhanced differentiation in response to serum starvation and retinoic acid. In contrast, overexpression of the catalytically inactive nm23-1T mutant enhanced TPA-mediated inhibition of differentiation. CONCLUSION: Our findings suggest that differentiation associated functions of nm23 proteins in IMR-32 neuroblastoma cells are carried out by bound nm23-1 proteins docked in a limited number of nm23-1 specific sites.
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