Abstract
In this issue of The American Journal of Pathology, long-time von Hippel-Lindau (VHL) pioneer William G. Kaelin with Nakamura and colleagues1 demonstrates that cells lacking wild-type VHL are defective in the expression and secretion of the glycoprotein clusterin. This phenomenon was observed in cells capable of ubiquitylating hypoxia-inducible factor (HIF) and possessing Type 2C VHL mutants. The authors also found that pVHL-defective renal carcinoma cells overexpress insulin-like growth factor binding protein-3 (IGBP3) and plasminogen activator inhibitor type-1 in a HIF-dependent manner. Previous reports have described pVHL modulating other genes in a HIF-independent manner to promote its tumor suppressor function; however, the overexpression of clusterin by pVHL raises several questions and requires further discussion.
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