A Juxtamembrane Basolateral Targeting Motif Regulates TGF-β Receptor Signaling in  Drosophila

2021 ◽  
Author(s):  
Aidan J. Peterson ◽  
Stephen J. Murphy ◽  
Melinda G. Mundt ◽  
MaryJane Shimell ◽  
Edward B. Leof ◽  
...  
Keyword(s):  
Receptor Signaling ◽  
Β Receptor ◽  
Basolateral Targeting

TGF-β receptor signaling and vascular biology

1998 ◽  
Vol 5 ◽  
pp. 170
Author(s):  
K. Miyazono ◽  
T. Imamura ◽  
M. Kato ◽  
A. Hanyu ◽  
M. Kawabata
Keyword(s):  
Vascular Biology ◽  
Receptor Signaling ◽  
Β Receptor

scholarly journals MED12 Controls the Response to Multiple Cancer Drugs through Regulation of TGF-β Receptor Signaling

Cell ◽  
2012 ◽  
Vol 151 (5) ◽  
pp. 937-950 ◽  
Author(s):  
Sidong Huang ◽  
Michael Hölzel ◽  
Theo Knijnenburg ◽  
Andreas Schlicker ◽  
Paul Roepman ◽  
...  
Keyword(s):  
Receptor Signaling ◽  
Cancer Drugs ◽  
Multiple Cancer ◽  
Β Receptor

scholarly journals Extracellular Matrix Derived from High Metastatic Human Breast Cancer Triggers Epithelial-Mesenchymal Transition in Epithelial Breast Cancer Cells through αvβ3 Integrin

2020 ◽  
Vol 21 (8) ◽  
pp. 2995 ◽  
Author(s):  
Renata Machado Brandão-Costa ◽  
Edward Helal-Neto ◽  
Andreza Maia Vieira ◽  
Pedro Barcellos-de-Souza ◽  
Jose Morgado-Diaz ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Extracellular Matrix ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Epithelial Mesenchymal Transition ◽  
Metastatic Breast ◽  
Receptor Signaling ◽  
Mesenchymal Transition ◽  
Β Receptor ◽  
Mcf 7

Alterations in the composition and architecture of the extracellular matrix (ECM) can influence cancer growth and dissemination. During epithelial-mesenchymal transition (EMT), epithelial cells assume a mesenchymal cell phenotype, changing their adhesion profiles from cell-cell contacts to cell-matrix interactions, contributing to metastasis. Breast cancer cells present at different stages of differentiation, producing distinct ECMs in the same tumor mass. However, the contribution of ECM derived from metastatic tumor cells to EMT is unclear. Here, we showed the mechanisms involved in the interaction of MCF-7, a low-metastatic, epithelial breast cancer cell line, with the ECM produced by a high metastatic breast tumor cell, MDA-MB-231 (MDA-ECM). MDA-ECM induced morphological changes in MCF-7 cells, decreased the levels of E-cadherin, up-regulated mesenchymal markers, and augmented cell migration. These changes were accompanied by the activation of integrin-associated signaling, with increased phosphorylation of FAK, ERK, and AKT and activation canonical TGF-β receptor signaling, enhancing phosphorylation of SMAD2 and SMAD4 nuclear translocation in MCF-7 cells. Treatment with Kistrin (Kr), a specific ligand of integrin αvβ3 EMT induced by MDA-ECM, inhibited TGF-β receptor signaling in treated MCF-7 cells. Our results revealed that after interaction with the ECM produced by a high metastatic breast cancer cell, MCF-7 cells lost their characteristic epithelial phenotype undergoing EMT, an effect modulated by integrin signaling in crosstalk with TGF-β receptor signaling pathway. The data evidenced novel potential targets for antimetastatic breast cancer therapies.

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