Matrix metalloproteinase (MMP) and TGF-β1-stimulated cell migration in skin and cornea wound healing

FAK mediates signal crosstalk between type II collagen and TGF-beta 1 cascades in chondrocytic cells

“…Highly increased FAK expression and cell migration were found in various malignant tumors including breast cancer, kidney cancer, osteosarcoma and chondrosarcoma (Golubovskaya et al, 2002;Golubovskaya et al, 2009;Jenq et al, 1996;Lee et al, 2003;Schroder et al, 2002;Tan et al, 2009). For invasion of cancer cells, the production of the ECM components such as type II collagen and GAGs, and expression of integrins, FAK and matrix metalloproteinases (MMPs) is necessary (Golubovskaya et al, 2009;Joo and Seomun, 2008;Lee et al, 2003). Cell proliferation and type II collagen expression were increased by type II collagen stimulation and reduced by FAK knockdown in normal human articular chondrocytes while GAG secretion remained unchanged (Kim and Lee, 2009).…”

Mesenchymal stem cell-derived CCL-9 and CCL-5 promote mammary tumor cell invasion and the activation of matrix metalloproteinases

“…36 Mostly, stroma-derived MMP-9 and MMP-13 and also tumor-derived MMP-1, MMP-2, and MMP-14 have been shown to contribute to invasive tumor growth and metastasis. [37][38][39] Given the complexity of the interactions between stroma and tumor cells within the breast tumor microenvironment, in vitro analyses of cell-cell interactions are essential models to provide a detailed understanding of the role of chemokines. Despite their no changes were noticed in the migration speed of 4T1 or NMuMG cells compared with the negative control (0% FBS) in monolayer repair over time measured following a 6 h incubation.…”

Prognostic significance of epidermal growth factor receptor and vascular endothelial growth factor receptor in colorectal adenocarcinoma

“…Mutations that activate EGFR are related to an increased response rate and survival in patients treated with EGFR tyrosine kinase inhibitors (4)(5)(6)(7)(8). In addition, the transactivation of EGFR is thought to regulate early transforming growth factor (TGF)-b signaling and may represent a novel pathway to control TGF-b-mediated gene expression (9). In animal models, EGFR inhibition enhances TGF-b-mediated apoptosis by increasing the oxidative stress response in cells (10).…”