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( 10 ). Cancer metastasis is facilitated by the remodeling of the extracellular matrix (ECM) at the tumor site ( 11 ) and during invasion of tissues ( 12 ). Breakdown of the ECM components is carried out by matrix metalloproteinases (MMPs), a family of
Centro de Investigaciones en Bioquímica Clínica e Inmunología (CIBICI-CONICET), Haya de la Torre y Medina Allende, Ciudad Universitaria, Córdoba (X5000HUA), Argentina
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Centro de Investigaciones en Bioquímica Clínica e Inmunología (CIBICI-CONICET), Haya de la Torre y Medina Allende, Ciudad Universitaria, Córdoba (X5000HUA), Argentina
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Instituto de Investigaciones en Ciencias de la Salud (INICSA-CONICET), Av. Enrique Barros y Enfermera Gordillo, Ciudad Universitaria, Córdoba, Argentina
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Centro de Investigaciones en Bioquímica Clínica e Inmunología (CIBICI-CONICET), Haya de la Torre y Medina Allende, Ciudad Universitaria, Córdoba (X5000HUA), Argentina
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another crucial step in cancer development. In these milieus, metalloproteinases (MMPs) play a relevant role by participating in the extracellular matrix (ECM) turnover and altering the cell-ECM and cell-cell interactions, causing tissue architecture
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tumors in distant organs ( 3 ). This process involves loss of cell-cell junctions and cell-extracellular matrix (ECM) interactions, acquisition of migratory capacity, matrix metalloproteases (MMPs) secretion, degradation of ECM and release from the
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Department of Veterinary Clinical and Animal Sciences, Novo Nordisk A/S, Department of Clinical Biochemistry, Department of Cardiothoracic and Vascular Surgery, Department of Clinical Biochemistry, Department of Veterinary Disease Biology, Department of Clinical Chemistry, Faculty of Health and Medical Sciences, University of Copenhagen, Frederiksberg C, Denmark
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metalloproteinases (MMPs), transforming growth factor β (TGFβ) isoforms, NOS, and natriuretic peptides (7, 8, 9, 10) . Moreover, microRNAs have emerged as new players in many developmental and pathological processes, i.e. cardiac development and heart hypertrophy
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. IL-6 neutralizing antibody was from R&D systems. Anti-total Stat3, anti-phospho Stat3 (p-Stat3), anti-Bcl-2, anti-myeloid cell leukemia-1 (Mcl-1), anti-CyclinD1, anti-matrix metalloproteinases 2 (MMP2) antibodies and rabbit IgG were from Epitomics (CA
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Guangdong Provincial Key Laboratory of Food, Nutrition and Health, Guangzhou, People’s Republic of China
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Guangdong Provincial Key Laboratory of Food, Nutrition and Health, Guangzhou, People’s Republic of China
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important role in the pathophysiological process. In the analysis of PPI network by the MCC method, the genes with top 10 MCC value were MYC, ANXA2, GDF15, AGTR1, NAMPT, LEPR, IGFBP-2, IL1RN, MMP7, and APLNR. The hub genes relationship in the STRING database
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cancer ( 4 , 40 , 41 ). We previously demonstrated that OA induces proliferation, invasion, MMP-9 secretion, activation of ERK1/2, FAK and Src, and an increase of AP1-DNA binding activity in breast cancer cells ( 8 , 9 , 10 ). However, the signal
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Department of Health & Life Sciences, Charles R. Drew University of Medicine and Science, Los Angeles, California, USA
Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, California, USA
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Department of Health & Life Sciences, Charles R. Drew University of Medicine and Science, Los Angeles, California, USA
Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, California, USA
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MSTN (−2.6). Continuous incubation of satellite cells with 1,25-D 3 also increased the expression of BMP4 (+2.7), a positive marker of myotube formation/maturation ( 29 ). In addition, MMP9 was upregulated (+3.2); MMP9 is a marker of myogenic cell
James P. Wilmot Cancer Institute, University of Rochester Medical Center, Rochester, New York, USA
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James Buchanan Brady Urological Institute, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
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James P. Wilmot Cancer Institute, University of Rochester Medical Center, Rochester, New York, USA
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James Buchanan Brady Urological Institute, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
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James P. Wilmot Cancer Institute, University of Rochester Medical Center, Rochester, New York, USA
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cell cycle progression and/or apoptosis in urothelial cells undergoing neoplastic transformation. In SVHUC-AR cells with MCA exposure, ATF2 knockdown significantly downregulated the expression of Bcl-2 , cyclin A2 , cyclin D1 , JUN and MMP-2
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metalloproteinases MMP2 and MMP9 was observed in the islets with microspheres ( n = 5–6, Fig. 4A and B ). No differences could be detected in the expression of the inhibitors tissue inhibitor of matrix metalloproteinases (TIMP) 1–3 between islet with or without