BORIS/CTCFL-mediated transcriptional regulation of the hTERT telomerase gene in testicular and ovarian tumor cells.

Détails

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Etat: Public
Version: de l'auteur
ID Serval
serval:BIB_53B2E2E10050
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
BORIS/CTCFL-mediated transcriptional regulation of the hTERT telomerase gene in testicular and ovarian tumor cells.
Périodique
Nucleic Acids Research
Auteur(s)
Renaud S., Loukinov D., Alberti L., Vostrov A., Kwon Y.W., Bosman F.T., Lobanenkov V., Benhattar J.
ISSN
1362-4962 (Electronic)
ISSN-L
0305-1048
Statut éditorial
Publié
Date de publication
2011
Volume
39
Numéro
3
Pages
862-873
Langue
anglais
Résumé
Telomerase activity, not detectable in somatic cells but frequently activated during carcinogenesis, confers immortality to tumors. Mechanisms governing expression of the catalytic subunit hTERT, the limiting factor for telomerase activity, still remain unclear. We previously proposed a model in which the binding of the transcription factor CTCF to the two first exons of hTERT results in transcriptional inhibition in normal cells. This inhibition is abrogated, however, by methylation of CTCF binding sites in 85% of tumors. Here, we showed that hTERT was unmethylated in testicular and ovarian tumors and in derivative cell lines. We demonstrated that CTCF and its paralogue, BORIS/CTCFL, were both present in the nucleus of the same cancer cells and bound to the first exon of hTERT in vivo. Moreover, exogenous BORIS expression in normal BORIS-negative cells was sufficient to activate hTERT transcription with an increasing number of cell passages. Thus, expression of BORIS was sufficient to allow hTERT transcription in normal cells and to counteract the inhibitory effect of CTCF in testicular and ovarian tumor cells. These results define an important contribution of BORIS to immortalization during tumorigenesis.
Pubmed
Web of science
Open Access
Oui
Création de la notice
22/03/2011 11:53
Dernière modification de la notice
20/08/2019 14:08
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