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RNAi profiling of human fibrosarcoma cell line knocked down for MT1-MMP

ABSTRACT: To define the role of MT1-MMP in the tumor progression, we suppressed its expression in human fibrosarcoma cell line, HT1080, using RNAi technique. The gene expression pattern was then compared betweent the two experimental cell groups with contrasting MT1-MMP expression level.

ORGANISM(S): Homo sapiens

SUBMITTER: Wei Zeng

PROVIDER: E-GEOD-1774 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Suppression of MT1-MMP in Human Fibrosarcoma Impair Tumor Angiogenesis and Enlargement

Project description:To define the role of MT1-MMP in the tumor progression, we suppressed its expression in human fibrosarcoma cell line, HT1080, using RNAi technique. The gene expression pattern was then compared betweent the two experimental cell groups with contrasting MT1-MMP expression level. Keywords: other

2008-09-01 | GSE1774 | GEO

MT1-MMP induces malignant transformation in Mammary cells

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MT1-MMP (MMP14)-dependent gene expression in APOE-null vascular smooth muscle cells (VSMCs)

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Inhibition of ß1 integrin induces its association with MT1-MMP and decreases MT1- MMP internalization and cellular invasiveness

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Expression array of early postnatal Mt1-mmp-targeted mammary glands

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Genome-wide analysis of MCF-7 cells expressing or not MMP-14 (MT1-MMP) growing in monolayer cell culture conditions

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Comparison of gene expression in mouse placentas with different combination of MT1-MMP and MT2-MMP alleles

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2010-03-09 | E-GEOD-18604 | biostudies-arrayexpress

Expression array of Mt1-mmp+/+ and Mt1-mmp-/- mouse macrophages in response to LPS or IL-4

Project description:Macrophages dominate inflammatory environments where they modify the extracellular matrix by mobilizing complex repertoires of proteolytic enzymes. Nevertheless, the dominant proteinases used by macrophage as they confront physiologic tissue barriers remain undefined. Herein, we have characterized the molecular mechanisms that define human macrophage-extracellular matrix interactions ex vivo. Resting and immune-polarized macrophages are shown to proteolytically remodel basement membranes while infiltrating the underlying interstitial matrix. In an unbiased screen to identify key proteases, we find that the macrophage metalloproteinase, MT1-MMP, is the dominant effector of basement membrane degradation and invasion. These studies not only identify MT1-MMP as a key proteolytic effector of extracellular matrix remodeling by human macrophages, but also define the invasive strategies used by macrophages to traverse physiologic tissue barriers.

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Extracellular Matrix Proteolysis by MT1-MMP is Associated with Influenza-Related Mortality

Project description:The balance between protecting tissue integrity and efficient immune response is critical for host survival. Here we investigate the role of extracellular matrix (ECM) proteolysis in achieving this balance in the lung during influenza virus infection using a combined genomic and proteomic approach. We followed the transcriptional dynamics and ECM- related responses in a mouse model of influenza virus infection, integrated with whole tissue imaging and functional assays. Our study identifies MT1-MMP as a prominent host-ECM-remodeling collagenase in influenza virus infection. We show that selective inhibition of MT1-MMP-driven ECM proteolysis protects the tissue from infection-related structural and compositional damage. Inhibition of MT1-MMP did not significantly alter the immune response or cytokine expression, indicating its dominant role in ECM remodeling. We demonstrate that the available treatment for influenza virus (Tamiflu/ Oseltamivir) does not prevent lung ECM damage and is less effective than anti-MT1-MMP treatment in influenza virus and Streptococcus pneumoniae coinfection paradigms. Importantly, combination therapy of Tamiflu with anti-MT1-MMP shows a strong synergistic effect and results in complete recovery in mice. This study highlights the importance of tissue tolerance agents for surviving infectious diseases, and the potential of such host-pathogen therapy combination for respiratory infections.

2017-01-01 | GSE85597 | GEO

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