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Dual contribution of MAPK and PI3K in epidermal growth factor-induced destabilization of thyroid follicular integrity and invasion of cells into extracellular matrix

Journal article
Authors Camilla Ingeson-Carlsson
Mikael Nilsson
Published in Experimental Cell Research
Volume 326
Issue 2
Pages 210-218
ISSN 0014-4827
Publication year 2014
Published at Sahlgrenska Cancer Center
Pages 210-218
Language en
Links dx.doi.org/10.1016/j.yexcr.2014.04....
Keywords Thyroid, EGF, Migration, EMT, MEK, PI3K, EPITHELIAL-MESENCHYMAL TRANSITION, BREAST-CANCER CELLS, PHOSPHATIDYLINOSITOL 3-KINASE, COLLAGEN GEL, FACTOR-BETA, SIGNALING, PATHWAYS, TUMOR PROGRESSION, PRIMARY CULTURE, RESISTANCE, MIGRATION, Oncology, Cell Biology
Subject categories Clinical Medicine

Abstract

Normal thyrocytes grown as reconstituted follicles in collagen gel were evaluated for drug effects of small molecule kinase inhibitors on growth factor-induced cell migration in a 3D context. MEK inhibition by U0126 only partially antagonized EGF/serum-induced cell migration from the basal follicular surface into the matrix. Combined treatment with U0126 and LY294002, a PI3K blocker, was necessary to abolish migration. However, exposure to only LY294002 facilitated the response to EGF by breakdown of the original follicular structure. In the same time EGF promoted thyroid cell survival that was compromised by LY294002 in absence of EGF. Cells treated with EGF and LY294002 retained the ability to form follicles. The findings indicate that dual inhibition of MAPK and PI3K/AKT pathways is required to fully block matrix invasion of EGF-stimulated thyroid cells. Conversely, single drug treatment with PI3K inhibitor adversely promotes invasiveness probably by destabilizing the follicular epithelium. (C) 2014 Elsevier Inc. All rights reserved.

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