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Invited Review

The role of von Hippel-Lindau tumor suppressor protein and hypoxia in renal clear cell carcinoma

¹Department of Laboratory Medicine and Pathobiology, Faculty of Medicine, University of Toronto, Toronto M5S 1A8; and ²Departments of Surgery (Urology) and Surgical Oncology, University of Toronto and Princess Margaret Hospital, University Health Network, Toronto, Ontario, Canada M5G 2M9

The majority of kidney cancers are caused by the mutation of the von Hippel-Lindau (VHL) tumor suppressor gene. VHL protein (pVHL) is part of an E3 ubiquitin ligase complex called VEC that is composed of elongin B, elongin C, cullin 2, NEDD8, and Rbx1. VEC targets a hypoxia-inducible factor (HIF) transcription factor for ubiquitin-mediated destruction selectively in the presence of oxygen. In the absence of wild-type pVHL, as in VHL patients or in the majority of sporadic clear cell renal cell carcinomas, HIF-responsive genes are inappropriately activated even under normoxia. Recent insights into the molecular mechanisms regulating the function of pVHL, and thereby HIF, in the context of kidney cancer are the focus of this review.

hypoxia-inducible factor; renal cell carcinoma; E3 ubiquitin ligase

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