Abstract:
:Loss of Fanconi anemia (FA) proteins activity by recessive inherited mutations in one of the FA genes leads to a disease characterized by bone marrow failure, myeloid leukemia and DNA damage hypersensitivity. The aim of this work was to improve our understanding of the FA syndrome defining the transcription profile of the FA complementation group C (FANCC)-deficient cells in comparison to their ectopically corrected counterpart using oligonucleotide microarrays. In this way, 49 RNAs have been isolated, which showed a consistent differential pattern of expression among FANCC mutated and corrected cells. The observed specific changes in gene expression suggest that FANCC regulates specifically myeloid differentiation and unmasks a previously unsuspected anti-inflammatory role for the FA proteins. In spite of the DNA damage hypersensitivity of the syndrome, no gene coding for a protein directly involved in DNA repair/damage response was found to be deregulated in our analysis. This observation suggests that FANCC does not directly control genes involved in DNA repair at the transcriptional level, but does not exclude a regulation at the translational or post-translational level, or by protein/protein interactions. The potential role of the differentially expressed genes in FA phenotype as well as a functional- and cellular-based clustering of the identified genes are presented and discussed.
journal_name
Oncogenejournal_title
Oncogeneauthors
Zanier R,Briot D,Dugas du Villard JA,Sarasin A,Rosselli Fdoi
10.1038/sj.onc.1207677subject
Has Abstractpub_date
2004-06-24 00:00:00pages
5004-13issue
29eissn
0950-9232issn
1476-5594pii
1207677journal_volume
23pub_type
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