Cited by 263Cancer, Hypoxia, and MetabolismRenal cell carcinoma treatmentEar and Head Tumors

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Regulation of E-cadherin Expression by VHL and Hypoxia-Inducible Factor

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Esteban, Miguel A., Tran, Maxine G.B., Harten, Sarah K., Hill, Peter, Castellanos, Maria C., Chandra, Ashish, Raval, Raju, O'Brien, Tim S., Maxwell, Patrick H.·2006·Cancer Research

DOI 10.1158/0008-5472.can-05-2670

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Abstract

Mutations in von Hippel-Lindau tumor suppressor gene (VHL) underlie the VHL hereditary cancer syndrome and also occur in most sporadic clear cell renal cell cancers (CCRCC). Currently, the mechanism(s) by which VHL loss of function promotes tumor development in the kidney are not fully elucidated. Here, we show that VHL inactivation in precancerous lesions in kidneys from patients with VHL disease correlates with marked down-regulation of the intercellular adhesion molecule E-cadherin. Moreover, in VHL-defective cell lines (RCC4 and RCC10) derived from sporadic CCRCC, reexpression of VHL was found to restore E-cadherin expression. The product of the VHL gene has multiple reported functions, the best characterized of which is its role as the recognition component of an ubiquitin E3 ligase complex responsible for mediating oxygen-dependent destruction of hypoxia-inducible factor-α (HIF-α) subunits. We show that HIF activation is necessary and sufficient to suppress E-cadherin in renal cancer cells. Given the fundamental role of E-cadherin in controlling epithelial behavior, our findings give insight into how VHL inactivation/HIF activation may lead to kidney cancer and also indicate a mechanism by which reduced oxygenation could alter E-cadherin expression in other cancers and influence normal homeostasis in other epithelia. (Cancer Res 2006; 66(7): 3567-75)

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Authors: Esteban, M. A., Tran, M. G. B., Harten, S. K., Hill, P., Castellanos, M. C., Chandra, A., Raval, R., O'Brien, T. S., & Maxwell, P. H.
Affiliations: Imperial College London (GB)
3Servicio de Immunología, Hospital de la Princesa, Universidad Autónoma de Madrid, Madrid, Spain; and
Guy's Hospital (GB)
4Henry Wellcome Building of Genomic Medicine, Oxford, United Kingdom
2Department of Urology, Guy's Hospital, London Bridge, London, United Kingdom;
ORCID: Esteban, Miguel A.
Tran, Maxine G.B.
Chandra, Ashish
Raval, Raju
Maxwell, Patrick H.
Venue: Cancer Research
Publisher: American Association for Cancer Research (AACR)
Published: 2006-04-01
Volume: 66
Issue: 7
Pages: 3567-3575
ISSN: 0008-5472 (ISSN-L)
1538-7445
DOI: 10.1158/0008-5472.can-05-2670
OpenAlex: W2039412091
Cited by: 262
References: 37
Citations by year: 2026: 2 · 2025: 3 · 2024: 7 · 2023: 6 · 2022: 6 · 2021: 6 · 2020: 7 · 2019: 7 · 2018: 10 · 2017: 5 · 2016: 14 · 2015: 14 · 2014: 18 · 2013: 17 · 2012: 19
FWCI: 10.34
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: Cancer Research (publishedVersion)
PubMed (publishedVersion)
UCL Discovery (University College London) (submittedVersion)
Funders: Wellcome Trust
European Commission
Medical Research Council
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
Health Sciences › Medicine › Oncology › Renal cell carcinoma treatment
Health Sciences › Medicine › Oncology › Ear and Head Tumors
Keywords: E-cadherin, von Hippel-Lindau tumor suppressor, hypoxia-inducible factor alpha, clear cell renal cell carcinoma, von Hippel-Lindau disease, cell-cell adhesion, epithelial cell adhesion, E3 ubiquitin ligase, tumor suppressor inactivation, oxygenation
MeSH terms: Adult, Carcinoma, Renal Cell, Cell Transformation, Neoplastic, Female, von Hippel-Lindau Disease, Humans, Kidney Neoplasms, Kidney Tubules, Male, Middle Aged, Precancerous Conditions, RNA, Messenger, Down-Regulation, Cadherins, Hypoxia-Inducible Factor 1, Von Hippel-Lindau Tumor Suppressor Protein

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Regulation of E-cadherin Expression by VHL and Hypoxia-Inducible Factor

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