DLC2 modulates angiogenic responses in vascular endothelial cells by regulating cell attachment and migration

Y. Lin, N. T. Chen, Y. P. Shih, Y. C. Liao, L. Xue, Su Hao Lo

Research output: Contribution to journalArticle

25 Scopus citations

Abstract

Deleted in liver cancer 1 (DLC1) is a RhoGTPase activation protein-containing tumor suppressor that associates with various types of cancer. Although DLC2 shares a similar domain structure with that of DLC1, the function of DLC2 is not well characterized. Here, we describe the expression and ablation of DLC2 in mice using a reporter-knockout approach. DLC2 is expressed in several tissues and in endothelial cells (ECs) of blood vessels. Although ECs and blood vessels show no histological abnormalities and mice appear overall healthy, DLC2-mutant mice display enhanced angiogenic responses induced by matrigel and by tumor cells. Silencing of DLC2 in human ECs has reduced cell attachment, increased migration, and tube formation. These changes are rescued by silencing of RhoA, suggesting that the process is RhoA pathway dependent. These results indicate that DLC2 is not required for mouse development and normal vessel formation, but may protect mouse from unwanted angiogenesis induced by, for example, tumor cells.

Original languageEnglish (US)
Pages (from-to)3010-3016
Number of pages7
JournalOncogene
Volume29
Issue number20
DOIs
StatePublished - May 20 2010

Keywords

  • Angiogenesis
  • DLC2
  • RhoGAP
  • Tumor suppressor

ASJC Scopus subject areas

  • Molecular Biology
  • Cancer Research
  • Genetics

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