Abstract
Inactivation of the von Hippel-Lindau tumor suppressor gene is linked to the development of hereditary (VHL Disease-associated) and sporadic clear cell carcinoma of the kidney. The VHL gene product, pVHL, targets the heterodimeric transcription factor HIF for polyubiquitination, and restoration of pVHL function in VHL-/- renal carcinoma cells suppresses their ability to form tumors in nude mice. Here we show that tumor suppression by pVHL can be overridden by a HIF variant that escapes pVHL control. These studies prove that HIF is a critical downstream target of pVHL and establish that activation of HIF target genes can promote tumorigenesis in vivo.
Original language | English (US) |
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Pages (from-to) | 237-246 |
Number of pages | 10 |
Journal | Cancer Cell |
Volume | 1 |
Issue number | 3 |
DOIs | |
State | Published - Apr 2002 |
Externally published | Yes |
ASJC Scopus subject areas
- Cancer Research
- Cell Biology
- Oncology