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Insufficient ability of Rac1b to perturb cystogenesis.

Abstract
Rac1b is frequently expressed in a number of human cancer cells. It is still unclear, however, whether Rac1b causes morphological abnormalities in epithelial tissues. To investigate whether Rac1b induces morphological changes in 3-dimensional epithelial structures, we utilized an auxin-dependent protein expression system, which enabled us to rapidly induce and evaluate Rac1b function in MDCK (Madin-Darby Canine Kidney) cysts, a model for polarized epithelial structure. Cells carrying the wild-type Rac1, Rac1b and constitutively active Rac1V12 gene were morphologically indistinguishable from normal, when their coding proteins were not expressed. However, upon protein induction, Rac1V12, but not the wild-type Rac1 or Rac1b, significantly induced the luminal cell accumulation. Live cell imaging with cell cycle indicators showed that expression of Rac1V12, but not the wild-type Rac1 or Rac1b, promoted cell cycle progression. From these results, we concluded that the expression of Rac1b per se cannot induce cell proliferation. Rather, it is considered that Rac1b expression may participate in progression of malignancy.
AuthorsYoshifumi Mori, Shunsuke Yagi, Atsuro Sakurai, Michiyuki Matsuda, Etsuko Kiyokawa
JournalSmall GTPases (Small GTPases) 2013 Jan-Mar Vol. 4 Issue 1 Pg. 9-15 ISSN: 2154-1256 [Electronic] United States
PMID23411476 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • rac1 GTP-Binding Protein
Topics
  • Animals
  • Cell Cycle
  • Cell Line
  • Cell Proliferation
  • Dogs
  • Epithelial Cells (cytology, metabolism)
  • Gene Expression
  • Humans
  • Neoplasms (genetics)
  • rac1 GTP-Binding Protein (genetics, metabolism)

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