Reference : Creb-1 and Ap-1 Transcription Factors Jund and Fra-2 Regulate Bone Sialoprotein Gene Exp...
Scientific journals : Article
Life sciences : Biochemistry, biophysics & molecular biology
Human health sciences : Oncology
http://hdl.handle.net/2268/24057
Creb-1 and Ap-1 Transcription Factors Jund and Fra-2 Regulate Bone Sialoprotein Gene Expression in Human Breast Cancer Cells
English
Detry, Cédric mailto [Université de Liège - ULg > Services généraux (Faculté de médecine) > Service administratif de la Faculté (Médecine) >]
Lamour, Virginie mailto [Université de Liège - ULg > > Centre facultaire de rech. en cancérologie expérimentale >]
Castronovo, Vincenzo mailto [Université de Liège - ULg > Département des sciences biomédicales et précliniques > Biologie générale et cellulaire >]
Bellahcene, Akeila mailto [Université de Liège - ULg > Département des sciences biomédicales et précliniques > Labo de recherche sur les métastases >]
Feb-2008
BONE
42
2
422-31
Yes (verified by ORBi)
International
8756-3282
[en] Bone sialoprotein ; CREB-1 ; JunD ; Fra-2 ; Breast cancer
[en] Bone sialoprotein (BSP) expression is detected in a variety of human osteotropic cancers. High expression of BSP in breast and prostate primary carcinomas is associated with progression and bone metastases development. In this study, we examined the transcriptional regulation of BSP gene expression in MDA-MB-231 and MCF-7 human breast cancer cells compared with Saos-2 human osteoblast-like cells. BSP human promoter deletion analyses delineated a -56/-84 region, which comprises a cAMP response element (CRE) that was sufficient for maximal promoter activity in breast cancer cell lines. We found that the basic fibroblast growth factor response element (FRE) also located in the proximal promoter was a crucial regulator of human BSP promoter activity in Saos-2 but not in breast cancer cells. Promoter activity experiments in combination with DNA mobility shift assays demonstrated that BSP promoter activity is under the control of the CRE element, through CREB-1, JunD and Fra-2 binding, in MDA-MB-231, MCF-7 and in Saos-2 cells. Forskolin, a protein kinase A pathway activator, failed to enhance BSP transcriptional activity suggesting that CRE site behaves as a constitutive rather than an inducible element in these cell lines. Over-expression of JunD and Fra-2 increased BSP promoter activity and upregulated endogenous BSP protein expression in MCF-7 and Saos-2 cells while siRNA-mediated inhibition of both factors expression significantly reduced BSP protein level in MDA-MB-231. Collectively, these data provide with new transcriptional mechanisms, implicating CREB and AP-1 factors, that control BSP gene expression in breast cancer cells.
Giga-Cancer
Fonds de la Recherche Scientifique (Communauté française de Belgique) - F.R.S.-FNRS ; TELEVIE ; Inter University Attraction Pole (IAP-P/31) ; European Commission (METABRE - STROMA)
http://hdl.handle.net/2268/24057
10.1016/j.bone.2007.10.016

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