Transcription Factor PROX1 Induces Colon Cancer Progression by Promoting the Transition from Benign to Highly Dysplastic Phenotype

Petrova, T. V., Nykanen, A., Norrmen, C., Ivanov, K. I., Andersson, L. C., Haglund, C., Puolakkainen, P., Wempe, F., Melchner, H. von, Gradwohl, G., Vanharanta, S., Aaltonen, L. A., Saharinen, J., Gentile, M., Clarke, Alan Richard ORCID: https://orcid.org/0000-0002-4281-426X, Taipale, J., Oliver, G. and Alitalo, K. 2008. Transcription Factor PROX1 Induces Colon Cancer Progression by Promoting the Transition from Benign to Highly Dysplastic Phenotype. Cancer Cell 13 (5) , pp. 407-419. 10.1016/j.ccr.2008.02.020

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Abstract

The Drosophila transcription factor Prospero functions as a tumor suppressor, and it has been suggested that the human counterpart of Prospero, PROX1, acts similarly in human cancers. However, we show here that PROX1 promotes dysplasia in colonic adenomas and colorectal cancer progression. PROX1 expression marks the transition from benign colon adenoma to carcinoma in situ, and its loss inhibits growth of human colorectal tumor xenografts and intestinal adenomas in Apcmin/+ mice, while its transgenic overexpression promotes colorectal tumorigenesis. Furthermore, in intestinal tumors PROX1 is a direct and dose-dependent target of the β-catenin/TCF signaling pathway, responsible for the neoplastic transformation. Our data underscore the complexity of cancer pathogenesis and implicate PROX1 in malignant tumor progression through the regulation of cell polarity and adhesion.

Item Type:	Article
Date Type:	Publication
Status:	Published
Schools:	Biosciences
Subjects:	Q Science > QH Natural history > QH426 Genetics Q Science > QL Zoology Q Science > QR Microbiology R Medicine > RC Internal medicine > RC0254 Neoplasms. Tumors. Oncology (including Cancer)
Uncontrolled Keywords:	Cell cycle
Publisher:	Cell Press
ISSN:	1535-6108
Last Modified:	18 Oct 2022 12:17
URI:	https://orca.cardiff.ac.uk/id/eprint/9258

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