Nm23-M2/NDP kinase B induces endogenous c-myc and nm23-M1/NDP kinase a overexpression in BAF3 cells. Both NDP kinases protect the cells from oxidative stress-induced death
Experimental Cell Research. 2004-12-01; 301(2): 293-304
DOI: 10.1016/j.yexcr.2004.07.026
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1. Exp Cell Res. 2004 Dec 10;301(2):293-304.
Nm23-M2/NDP kinase B induces endogenous c-myc and nm23-M1/NDP kinase A
overexpression in BAF3 cells. Both NDP kinases protect the cells from oxidative
stress-induced death.
Arnaud-Dabernat S(1), Masse K, Smani M, Peuchant E, Landry M, Bourbon PM, Le
Floch R, Daniel JY, Larou M.
Author information:
(1)Laboratoire de Biologie de la Différenciation et du Développement, Université
Victor Segalen Bordeaux 2, EA 3674, 33076 Bordeaux cedex, France.
The nm23 gene family encodes nucleoside diphosphate kinases (NDPKs) which supply
the cell with (d)NTPs. The human NDPKB, also known as the PuF protein, binds the
c-myc promoter and transactivates the c-myc protooncogene. We have now studied
the effects of mouse NDPKA and NDPKB overexpression on endogenous c-myc
transactivation in the mouse BAF3 and the rat PC12 cell lines. c-myc transcripts
were found to be up-regulated by NDPKB only in the BAF3 line. This suggests that
c-myc transcriptional control via NDPKB depends on the presence of cell-specific
co-factors. Unexpectedly, NDPKB also induced NDPKA expression. This new effect
was found in both cell lines, suggesting that NDPKB-dependent nm23-M1 gene
transactivation requires cis and/or trans elements different from those involved
in c-myc transactivation. Moreover, the BAF3 cell proliferation capacities were
found to be independent of NDPKA or B cell contents. Interestingly, cell death
induced by c-myc overexpression or H(2)O(2) exposure was decreased in
nm23-transfected compared to control BAF3 cells. These data collectively suggest
that NDPKs might improve cell survival by a mechanism coupling DNA repair and
transcriptional regulation of genes involved in DNA damage response.
DOI: 10.1016/j.yexcr.2004.07.026
PMID: 15530864 [Indexed for MEDLINE]