Over expression of endoglin in human prostate cancer suppresses cell detachment, migration and invasion

Yuequin Liu, Borko Jovanovic, Michael Pins, Chung Lee, Raymond C. Bergan

Research output: Contribution to journalArticle

90 Scopus citations

Abstract

The regulation of cell adhesion and motility in human prostate is not well understood. We have previously shown that the endoglin gene is differently expressed during changes in prostate cell adhesion. Endoglin is a transmembrane transforming growth factor β binding protein typically expressed by endothelial cells. In this report we demonstrate that endoglin over expression increases prostate cell attachment, while decreasing migration and invasion. Engineered decreases in endoglin expression have opposite effects. While endoglin exerted only relatively small effects upon cell adhesion, large effects upon cell migration and invasion were observed. Endoglin was shown to localize to focal adhesion plaques, consistent with its role in regulating cell adhesion and motility. Loss of endoglin expression in cancer, as compared to normal prostate, was seen in human prostate cell lines. Suppression of endoglin expression in a panel of normal human prostate cell lines led to cell detachment. Endoglin is identified as a regulator of cell adhesion, motility and invasion in human prostate. Loss of endoglin expression appears to be associated with prostate cancer progression, at least in vitro.

Original languageEnglish (US)
Pages (from-to)8272-8281
Number of pages10
JournalOncogene
Volume21
Issue number54
DOIs
StatePublished - Nov 28 2002

Keywords

  • Adhesion
  • Carcinogenesis
  • Motility
  • Transforming growth factor beta

ASJC Scopus subject areas

  • Molecular Biology
  • Genetics
  • Cancer Research

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