原创力文档rearrangements of the actin cytoskeleton and e-cadherin–based adherens junctions caused by neoplasic transformation change cell–cell interactions肌动蛋白细胞骨架重组和e-cadherin-based neoplasic引起粘合连接处并且转换变化和信息交互.pdfVIP
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rearrangements of the actin cytoskeleton and e-cadherin–based adherens junctions caused by neoplasic transformation change cell–cell interactions肌动蛋白细胞骨架重组和e-cadherin-based neoplasic引起粘合连接处并且转换变化和信息交互
Rearrangements of the Actin Cytoskeleton and
E-Cadherin–Based Adherens Junctions Caused by
Neoplasic Transformation Change Cell–Cell Interactions
. .
Dmitry V. Ayollo , Irina Y. Zhitnyak , Jury M. Vasiliev, Natalya A. Gloushankova*
Institute of Carcinogenesis, N.N. Blokhin Cancer Research Center of the Russian Academy of Medical Sciences, Moscow, Russia
Abstract
E-cadherin–mediated cell–cell adhesion, which is essential for the maintenance of the architecture and integrity of epithelial
tissues, is often lost during carcinoma progression. To better understand the nature of alterations of cell–cell interactions at
the early stages of neoplastic evolution of epithelial cells, we examined the line of nontransformed IAR-2 epithelial cells and
their descendants, lines of IAR-6-1 epithelial cells transformed with dimethylnitrosamine and IAR1170 cells transformed with
N-RasG12D. IAR-6-1 and IAR1170 cells retained E-cadherin, displayed discoid or polygonal morphology, and formed
monolayers similar to IAR-2 monolayer. Fluorescence staining, however, showed that in IAR1170 and IAR-6-1 cells the
marginal actin bundle, which is typical of nontransformed IAR-2 cells, disappeared, and the continuous adhesion belt
(tangential adherens junctions (AJs)) was replaced by radially oriented E-cadherin–based AJs. Time-lapse imaging of IAR-6-1
cells stably transfected with GFP-E-cadherin revealed that AJs in transformed cells are very dynamic and unstable. The
regulation of AJ assembly by Rho family small GTPases was different in nontransformed and in transformed IAR epithelial
cells. As our experiments with the ROCK inhibitor Y-27632 and the myosin II inhibitor blebbistatin have shown, the
formation and maintenance of radial AJs critic
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