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Papers In Press, published online ahead of print December 15, 2004
J. Biol. Chem, 10.1074/jbc.M413248200
Submitted on November 23, 2004
Revised on December 14, 2004
Accepted on December 15, 2004
Department of Pediatrics, University of Sherbrooke, Sherbrooke, Quebec J1H 5N4
Corresponding Author: claire.m.dubois{at}usherbrooke.ca
Hypoxia is a common tumorigenesis enhancer, mostly owing to its impact on gene expression of many angiogenic and invasion-related mediators, some of which are natural substrates for the proprotein convertase furin. Analysis of furin promoters revealed the presence of putative binding sites for HIF-1, a transcription complex that plays a pivotal role in cellular adaptation to hypoxia. In fact, we demonstrate herein that the levels of fur mRNA, encoding furin, are remarkably increased upon hypoxic challenge. Co-transfection of a HIF-1a DN in WT cells or transfection of a furin promoter-reporter gene in HIF-1-deficient cells indicated the requirement of HIF-1 for furin promoter activation by hypoxia. Direct HIF-1 action on the furin promoter was identified as a canonical HRE site with enhancer capability. The hypoxic/HIF-1 regulation of furin correlated with an increased proteolytic activation of the substrates MT1-MMP and TGFb1. Our findings unveil a new facet of the physiological consequences of hypoxia/HIF-1, through enhanced furin-induced proteolytic processing/activation of proproteins known to be involved in tumorigenesis.
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