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  • 1
    Keywords: RECEPTOR ; CELLS ; EXPRESSION ; GROWTH ; GROWTH-FACTOR ; IN-VITRO ; INVASION ; tumor ; TUMOR-CELLS ; Germany ; VITRO ; SYSTEM ; SYSTEMS ; ENZYMES ; TISSUE ; MECHANISM ; FAMILY ; INDUCTION ; mechanisms ; fibroblasts ; ALPHA ; antibodies ; antibody ; PROGRESSION ; METASTASIS ; NUDE-MICE ; MELANOMA ; DEGRADATION ; ANTAGONIST ; HUMAN DERMAL FIBROBLASTS ; MATRIX ; TUMOR INVASION ; collagen ; MATRIX METALLOPROTEINASES ; MELANOMA-CELLS ; TUMORIGENICITY ; regulation ; interaction ; basic fibroblast growth factor ; bFGF ; dermal fibroblasts ; IL-1 alpha ; MALIGNANT MELANOMAS ; TIMP-1 ; TISSUE INHIBITOR
    Abstract: Tumor invasion and metastasis of melanoma have been shown to require proteolytic degradation of the extracellular environment, achieved primarily by enzymes of the matrix metalloproteinases (MMP) family. Increased enzyme activity is localized at the border of tumor cells and the adjacent peritumoral connective tissue, emphasizing the crucial role of tumor-stroma interactions in the regulation of MMP activity. To analyze whether direct cell-cell contacts of melanoma cells and stromal fibroblasts or whether soluble factors, secreted by melanoma cells are involved in the regulation of MMP, we used different in vitro co-culture systems. Both direct and indirect co-cultures of high invasive BLM melanoma cells and human dermal fibroblasts resulted in an induction of pro-MMP-1 synthesis. Medium conditioned by BLM cells strongly induced pro-MMP-1 synthesis in fibroblasts, indicating the importance of diffusible factors for this induction. Competition by recombinant human interleukin (IL)-1 receptor antagonist, neutralizing IL-1alpha and basic fibroblast growth factor (bFGF) antibodies, resulted in a concentration-dependent reduction of pro-MMP-1 synthesis. Taken together, our results indicate an essential role for soluble factors, mainly IL-1alpha and bFGF, in the stimulation of dermal fibroblasts by human melanoma cells to secrete MMP-1
    Type of Publication: Journal article published
    PubMed ID: 15737206
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  • 2
    Keywords: CELLS ; EXPRESSION ; GROWTH ; IN-VITRO ; proliferation ; Germany ; VITRO ; SYSTEM ; transcription ; DIFFERENTIATION ; TISSUE ; MICE ; ACTIVATION ; COMPLEX ; COMPLEXES ; FAMILY ; TRANSCRIPTION FACTOR ; KERATINOCYTES ; SKIN ; C-JUN ; fibroblasts ; treatment ; SIGNAL ; TRANSGENIC MICE ; STRESS ; REPAIR ; EPITHELIAL-CELLS ; KINETICS ; REGULATOR ; COLONY-STIMULATING FACTOR ; INTERCELLULAR COMMUNICATION ; TISSUE-SPECIFIC EXPRESSION ; inflammation ; CYTOKINE ; FAMILIES ; MICE LACKING ; KERATINOCYTE DIFFERENTIATION ; IMMUNE-SYSTEM ; LEVEL ; REGULATED GENE ; macrophage ; inflammatory cells ; COLLAGEN GEL ; GROWTH-STIMULATORY ACTIVITY ; TRANSCRIPTION FACTOR AP-1
    Abstract: The cutaneous response to injury and stress comprises a temporary change in the balance between epidermal proliferation and differentiation as well as an activation of the immune system. Soluble factors play an important role in the regulation of these complex processes by coordinating the intercellular communication between keratinocytes, fibroblasts, and inflammatory cells. In this study, we demonstrate that JunB, a member of the activator protein-1 transcription factor family, is an important regulator of cytokine expression and thus critically involved in the cutaneous response to injury and stress. Mice lacking JunB in the skin develop normally, indicating that JunB is neither required for cutaneous organogenesis, nor homeostasis. However, upon wounding and treatment with the phorbol ester 12-O-decanoyl-phorbol-13-acetate, JunB-deficiency in the skin likewise resulted in pronounced epidermal hyperproliferation, disturbed differentiation, and prolonged inflammation. Furthermore, delayed tissue remodelling was observed during wound healing. These phenotypic skin abnormalities were associated with JunB-dependent alterations in expression levels and kinetics of important mediators of wound repair, such as granulocyte macrophage colony-stimulating factor, growth-regulated protein-1, macrophage inflammatory protein-2, and lipocalin-2 in both the dermal and epidermal compartment of the skin, and a reduced ability of wound contraction of mutant dermal fibroblasts in vitro
    Type of Publication: Journal article published
    PubMed ID: 16439969
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  • 3
    Keywords: USA ; NEW-YORK ; INVASION ; METASTASIS ; MELANOMA
    Type of Publication: Meeting abstract published
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  • 4
    Keywords: ENVIRONMENT ; CELLS ; EXPRESSION ; GROWTH ; INVASION ; tumor ; TUMOR-CELLS ; BLOOD ; CELL ; Germany ; LUNG ; imaging ; SUPPORT ; liver ; ENZYMES ; TISSUE ; TUMORS ; MICE ; TIME ; FAMILY ; animals ; INJECTION ; MAGNETIC-RESONANCE ; magnetic resonance imaging ; METASTASIS ; inactivation ; MELANOMA ; DEGRADATION ; MALIGNANT-MELANOMA ; melanoma cells ; PERMEABILITY ; MATRIX ; FAMILIES ; TUMOR INVASION ; TUMOR-GROWTH ; MATRIX METALLOPROTEINASES ; MELANOMA-CELLS ; regulation ; interaction ; INVASIVENESS ; lungs ; tumor stroma ; METALLOPROTEINASES ; matrix metalloproteinase ; Mice,Inbred C57BL ; Extracellular ; CONNECTIVE-TISSUE ; ENZYME-ACTIVITY ; tumor-stroma interaction ; Endothelial Cells/enzymology/pathology ; Gene Expression Regulation,Enzymologic/physiology ; Macrophages/pathology ; Matrix Metalloproteinase 13/*genetics/metabolism ; Melanoma/immunology/*physiopathology/*secondary ; Mice,Mutant Strains ; molecular medicine ; Neoplasm Transplantation ; Neovascularization,Pathologic/immunology/pathology/physiopathology ; Neutrophils/pathology ; Skin Neoplasms/immunology/*pathology/*physiopathology ; Stromal Cells/enzymology/pathology
    Abstract: Tumor invasion and metastasis of malignant melanoma have been shown to require proteolytic degradation of the extracellular environment achieved primarily by enzymes of the matrix metalloproteinases (MMP) family. We have earlier shown that increased enzyme activity is localized at the border of tumor cells and the adjacent peritumoral connective tissue, emphasizing the importance of tumor-stroma interactions in the regulation of MMP activity. To confirm the role of stroma-derived MMP-13 in the invasion process, we investigated the invasiveness of melanoma cells upon intradermal injection in mice with complete inactivation of MMP-13. Tumor growth was significantly impaired in mmp-13(-/-) mice and most significant at early time points as compared with wild-type littermates. Moreover, metastasis to various organs was reduced to 17.6 vs 30% in lungs, 2.9 vs 30% in the liver. Strikingly, ablation of MMP-13 completely abrogated formation of metastasis in the heart (0 vs 40%). Notably, decreased tumor growth in mmp-13(-/-) mice was associated with reduced blood vessel density. In addition, decreased blood vessel permeability in the tumors was measured by magnetic resonance imaging of tumor-bearing animals. These data suggest an important role of MMP-13 in tumor growth and an unexpected role in organ-specific metastasis of melanoma cells.
    Type of Publication: Journal article published
    PubMed ID: 19516266
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  • 5
    ISSN: 0014-4827
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Medicine
    Type of Medium: Electronic Resource
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