We are analyzing https://link.springer.com/article/10.1007/s10911-010-9177-x.

Title:
Matrix Metalloproteinase-Induced Epithelial-Mesenchymal Transition in Breast Cancer | Journal of Mammary Gland Biology and Neoplasia
Description:
Matrix metalloproteinases (MMPs) degrade and modify the extracellular matrix (ECM) as well as cell-ECM and cell-cell contacts, facilitating detachment of epithelial cells from the surrounding tissue. MMPs play key functions in embryonic development and mammary gland branching morphogenesis, but they are also upregulated in breast cancer, where they stimulate tumorigenesis, cancer cell invasion and metastasis. MMPs have been investigated as potential targets for cancer therapy, but clinical trials using broad-spectrum MMP inhibitors yielded disappointing results, due in part to lack of specificity toward individual MMPs and specific stages of tumor development. Epithelial-mesenchymal transition (EMT) is a developmental process in which epithelial cells take on the characteristics of invasive mesenchymal cells, and activation of EMT has been implicated in tumor progression. Recent findings have implicated MMPs as promoters and mediators of developmental and pathogenic EMT processes in the breast. In this review, we will summarize recent studies showing how MMPs activate EMT in mammary gland development and in breast cancer, and how MMPs mediate breast cancer cell motility, invasion, and EMT-driven breast cancer progression. We also suggest approaches to inhibit these MMP-mediated malignant processes for therapeutic benefit.
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Keywords {🔍}

pubmed, google, scholar, cas, mmp, cancer, breast, mmps, cells, matrix, mammary, cell, emt, epithelial, metalloproteinase, tumor, biol, expression, metalloproteinases, progression, inhibitors, domain, activation, mtmmp, chem, tissue, development, gland, epithelialmesenchymal, invasion, mice, transition, res, morphogenesis, catalytic, branching, metastasis, studies, human, carcinoma, binding, model, inhibitor, migration, stromal, selective, therapeutic, membrane, radisky, invasive,

Topics {✒️}

tgf-beta-induced transcriptional activation transforming growth factor-beta transforming growth factor-beta1 producing epithelial-mesenchymal transformations rho-gdp dissociation inhibitors early-stage breast cancer jak/stat pathway activation natural mmp-inhibiting timps osteoclast-derived matrix metalloproteinase-7 node-positive breast cancer abl tyrosine kinase long-term oxidative stress tumor-induced host response cell-cell junction proteins stromelysin-1-dependent invasive properties tolerated mmp-directed therapeutics mmtv-pymt tumorigenesis model large-scale transcriptional profiling genome-wide transcript analysis discover selective drugs mmtv-driven mmp-3 expression stromal bone-resorbing osteoclasts tissue-specific gene expression epithelial-mesenchymal transition drug anti-targets due irreversible mechanism-based inhibitors computational time-lapse study early avian cardiac stromal cell-produced morphogen ras signaling pathways emt-driven tumor progression protease activated receptor-1 emt-related tissue morphogenesis combat mmp-mediated emt article download pdf focal adhesion kinase synthetic inhibitors developed targeting mmp-induced emt type iv collagen mcf-7 cells induced timp-1n-terminal domain epithelial-mesenchymal transformation mmp-mediated malignant processes matrix metalloproteinase inhibitors structure-based drug design enhances tyrosine phosphorylation retinoic acid signaling promotes cell migration synthetic pharmaceutical inhibitors phase iii trial

Questions {❓}

Can genes for mammographic density inform cancer aetiology?
Fibrosis and cancer: do myofibroblasts come also from epithelial cells via EMT?
MMPs as therapeutic targets-still a viable option?
Structural and functional bases for allosteric control of MMP activities: Can it pave the path for selective inhibition?

Schema {🗺️}

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         headline:Matrix Metalloproteinase-Induced Epithelial-Mesenchymal Transition in Breast Cancer
         description:Matrix metalloproteinases (MMPs) degrade and modify the extracellular matrix (ECM) as well as cell-ECM and cell-cell contacts, facilitating detachment of epithelial cells from the surrounding tissue. MMPs play key functions in embryonic development and mammary gland branching morphogenesis, but they are also upregulated in breast cancer, where they stimulate tumorigenesis, cancer cell invasion and metastasis. MMPs have been investigated as potential targets for cancer therapy, but clinical trials using broad-spectrum MMP inhibitors yielded disappointing results, due in part to lack of specificity toward individual MMPs and specific stages of tumor development. Epithelial-mesenchymal transition (EMT) is a developmental process in which epithelial cells take on the characteristics of invasive mesenchymal cells, and activation of EMT has been implicated in tumor progression. Recent findings have implicated MMPs as promoters and mediators of developmental and pathogenic EMT processes in the breast. In this review, we will summarize recent studies showing how MMPs activate EMT in mammary gland development and in breast cancer, and how MMPs mediate breast cancer cell motility, invasion, and EMT-driven breast cancer progression. We also suggest approaches to inhibit these MMP-mediated malignant processes for therapeutic benefit.
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      headline:Matrix Metalloproteinase-Induced Epithelial-Mesenchymal Transition in Breast Cancer
      description:Matrix metalloproteinases (MMPs) degrade and modify the extracellular matrix (ECM) as well as cell-ECM and cell-cell contacts, facilitating detachment of epithelial cells from the surrounding tissue. MMPs play key functions in embryonic development and mammary gland branching morphogenesis, but they are also upregulated in breast cancer, where they stimulate tumorigenesis, cancer cell invasion and metastasis. MMPs have been investigated as potential targets for cancer therapy, but clinical trials using broad-spectrum MMP inhibitors yielded disappointing results, due in part to lack of specificity toward individual MMPs and specific stages of tumor development. Epithelial-mesenchymal transition (EMT) is a developmental process in which epithelial cells take on the characteristics of invasive mesenchymal cells, and activation of EMT has been implicated in tumor progression. Recent findings have implicated MMPs as promoters and mediators of developmental and pathogenic EMT processes in the breast. In this review, we will summarize recent studies showing how MMPs activate EMT in mammary gland development and in breast cancer, and how MMPs mediate breast cancer cell motility, invasion, and EMT-driven breast cancer progression. We also suggest approaches to inhibit these MMP-mediated malignant processes for therapeutic benefit.
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