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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)

Project description:VSMC-specific MT1-MMP gene targeting in APOE-null mice promotes atherosclerosis and iliac artery aneurysm formation. To determine the MT1-MMP-dependent regulation of VSMC function, whole-genome transcriptomes of wild-type and MT1-MMP-null APOE-null VSMCs were determined. We used microarray-based transcriptome analysis to detect MT1-MMP-dependent regulation of VSMC function under atherogenic conditions.

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

Project description:Integrin signaling plays a fundamental role in the establishment of focal adhesions and the subsequent formation of invadopodia in malignant cancer cells. Invadopodia facilitate localized adhesion and degradation of the extracellular matrix (ECM), which promote tumour cell invasion and metastasis. Degradation of ECM components is often driven by membrane type-1 matrix metalloproteinase (MT1-MMP), and we have recently shown that regulation of enzyme internalization is dependent on signaling downstream of β1 integrin. Phosphorylation of the cytoplasmic tail of MT1-MMP is required for its internalization and delivery to Rab5-marked early endosomes, where it is then able to be recycled to new sites of invadopodia formation and promote invasion. Here we found that inhibition of β1 integrin, using the antibody AIIB2, inhibited the internalization and recycling of MT1-MMP that is necessary to support long-term cellular invasion. MT1-MMP and β1 integrin were sequestered at the cell surface when β1-integrin was inhibited, and their association under these conditions was detected using immunoprecipitation and mass spectrometry analysis. Sequestration of β1 integrin and MT1-MMP at the cell surface resulted in the formation of large invadopodia and local ECM degradation; however, the impaired internalization and recycling of MT1-MMP and β1 integrin ultimately led to a loss of invasive behaviour.

2022-12-22 | PXD024000 | Pride

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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2015-12-11 | GSE64320 | GEO

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.

2019-05-01 | GSE122823 | GEO

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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