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Transcriptional regulation Lemmens et al. (2001) RUNX2 (BMP2 signaling) Transcriptional regulation Sowa et al. (2004) SMADs (TGFβ signaling) (SMAD1, SMAD3, SMAD5) Transcriptional regulation Sowa et al. (2004) SIRT1
Division of Endocrinology, Diabetes, Metabolism and Nutrition, Mayo Clinic, Rochester, Minnesota, USA
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Division of Medical Oncology, Mayo Clinic, Rochester, Minnesota, USA
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/g) as compared to non-irradiated tumors (5.3 % ID/g) ( Schug et al. 2018 ). These data suggested that EBRT may not only enhance the migratory behavior of MSCs but may also act to potentially amplify activation of the TGFβ1-inducible SMAD
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proliferation. In ATC cells, NOTCH1 knockdown reduced miR-19. SMAD4 was validated as a miR-19 target by luciferase assay, which revealed reduced luminescence associated with miR-19–Smad4 3′-UTR interaction. Moreover, this effect was mimicked in PTC cells
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its effect through heterotrimeric complex of transmembrane serine/threonine kinase, the type I (RI) and type II (RII) receptors. Following ligand binding, RI phosphorylates Smad2 and Smad3 (R-Smads). Phosphorylated R-Smads form a complex with Smad4 and
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Department of Surgery and Cancer, Cardiff University School of Medicine, Imperial College London, Imperial Centre for Translational and Experimental Medicine, Du Cane Road, London W12 0NN, UK
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. 1993 ). Later it was shown that the C. elegans let7 gene product, also an ncRNA, could associate with the 3′-UTR of target genes to initiate a cascade of regulatory processes acting on heterochronic genes ( Reinhart et al . 2000 ). The
Division of Gastroenterology, Department of Medicine, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
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downregulation may enhance tumor cell proliferation, apoptosis and cell cycle progression by inhibiting miR-16’s target activity on the 3′-UTR of oncogenes such as Bcl-2, Smad3 and Yap-1 ( Cimmino et al . 2005 , Kang et al . 2015 , Zhang et al . 2018
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following gene sets: GCM_RAP2A ( Fig. 5C ), PID_SMAD2_3PATHWAY ( Fig. 5D ), and PID_WNT_CANONICAL_PATHWAY ( Fig. 5E ), which are associated with metastasis of certain cancers. Moreover, the CD39 lo PD-1 lo CD103 hi effector Tregs hi group upregulated the
Laboratory of Molecular Oncology, School of Molecular Medicine, Institut Gustave Roussy, Emory University School of Medicine, Department of Oncology, Military Institute of Medicine, Szaserow 128, 04‐141 Warsaw, Poland
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Laboratory of Molecular Oncology, School of Molecular Medicine, Institut Gustave Roussy, Emory University School of Medicine, Department of Oncology, Military Institute of Medicine, Szaserow 128, 04‐141 Warsaw, Poland
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Caki-2 cells. They also demonstrated that IGF1, through activation of Smad2 protein phosphorylation and its nuclear translocation, enhances TGF-β signaling, which in turn promotes IGFBP3 production. Such interconnection between IGFBP3 expression and
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more than 85% ( Fagin & Wells 2016 ). ATC is the most aggressive and deadly thyroid cancer accounting for less than 3% and its overall survival rate is only 3–5 months after initial diagnosis ( Fagin & Wells 2016 , Howlader et al. 2017 ). Currently
Translational Research Unit, Endocrine Neoplasia and Hormonal Disorders, Experimental Therapeutics, Department of Oncology, Hospital of Prato and Istituto Toscana Tumori, Piazza dell' Ospedale, 59100 Prato, Italy Departments of
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2 could be regulated by HMGA2, and that the regulation of Snail promoter by HMGA2 involves binding of this factor to Smad3 and Smad4 ( Thuault et al . 2008 ). In addition, RAS, which is another target of let-7 and a driving force for EMT, has