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Chemokine receptor CXCR4 downregulated by von Hippel-Lindau tumour suppressor pVHL.

Abstract：

:Organ-specific metastasis is governed, in part, by interactions between chemokine receptors on cancer cells and matching chemokines in target organs. For example, malignant breast cancer cells express the chemokine receptor CXCR4 and commonly metastasize to organs that are an abundant source of the CXCR4-specific ligand stromal cell-derived factor-1alpha (ref. 1). It is still uncertain how an evolving tumour cell is reprogrammed to express CXCR4, thus implementing the tendency to metastasize to specific organs. Here we show that the von Hippel-Lindau tumour suppressor protein pVHL negatively regulates CXCR4 expression owing to its capacity to target hypoxia-inducible factor (HIF) for degradation under normoxic conditions. This process is suppressed under hypoxic conditions, resulting in HIF-dependent CXCR4 activation. An analysis of clear cell renal carcinoma that manifests mutation of the VHL gene in most cases revealed an association of strong CXCR4 expression with poor tumour-specific survival. These results suggest a mechanism for CXCR4 activation during tumour cell evolution and imply that VHL inactivation acquired by incipient tumour cells early in tumorigenesis confers not only a selective survival advantage but also the tendency to home to selected organs.

journal_name

Nature

journal_title

Nature

authors

Staller P,Sulitkova J,Lisztwan J,Moch H,Oakeley EJ,Krek W

doi

10.1038/nature01874

keywords:

subject

Has Abstract

pub_date

2003-09-18 00:00:00

pages

307-11

issue

6955

eissn

0028-0836

issn

1476-4687

pii

nature01874

journal_volume

425

pub_type

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