Abstract
Lysyl Oxidase at the Crossroads of Mesenchymal Stem Cells and Epithelial-Mesenchymal Transition
Highlights
Breast carcinoma development is governed by dynamic interactions that operate between mutant cancer cells and the stromal compartments around them, which encompass a collection of mesenchymal cell types, such as endothelial cells, fibroblasts, and immune cells [1]
We have previously shown that certain progenitor cells called mesenchymal stem cells (MSCs), which otherwise contribute to the maintenance and regeneration of connective tissues under normal and inflammatory conditions, are incorporated into the stroma of developing tumors
We showed that the interactions of stromal MSCs with breast cancer cells within primary tumors activate the MSCs, which act back on the cancer cells in a paracrine fashion, increasing their motility, invasion, and metastasis [2]
Summary
Breast carcinoma development is governed by dynamic interactions that operate between mutant cancer cells and the stromal compartments around them, which encompass a collection of mesenchymal cell types, such as endothelial cells, fibroblasts, and immune cells [1]. We showed that the interactions of stromal MSCs with breast cancer cells within primary tumors activate the MSCs, which act back on the cancer cells in a paracrine fashion, increasing their motility, invasion, and metastasis [2]. We found that LOX caused robust induction of epithelial-mesenchymal transition (EMT) in the cancer cells, primarily by inducing the expression of the master transcription factor Twist.
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