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Sunita K Agarwal Metabolic Diseases Branch National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, Maryland, USA

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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

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C Spitzweg Department of Internal Medicine IV, University Hospital of LMU Munich, Munich, Germany
Division of Endocrinology, Diabetes, Metabolism and Nutrition, Mayo Clinic, Rochester, Minnesota, USA

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P J Nelson Department of Internal Medicine IV, University Hospital of LMU Munich, Munich, Germany

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E Wagner Pharmaceutical Biotechnology, Department of Pharmacy, Centre for System-Based Drug Research, and Centre for Nanoscience, LMU Munich, Munich, Germany

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P Bartenstein Department of Nuclear Medicine, University Hospital of LMU Munich, Munich, Germany

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W A Weber Department of Nuclear Medicine, Klinikum rechts der Isar, Technical University Munich, Munich, Germany

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M Schwaiger Department of Nuclear Medicine, Klinikum rechts der Isar, Technical University Munich, Munich, Germany

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J C Morris Division of Endocrinology, Diabetes, Metabolism and Nutrition, Mayo Clinic, Rochester, Minnesota, USA
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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Zhenying Guo Department of Pathology and Laboratory Medicine, University of Wisconsin School of Medicine and Public Health, Zhejiang, China

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Heather Hardin Department of Pathology and Laboratory Medicine, University of Wisconsin School of Medicine and Public Health, Zhejiang, China

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Ricardo V Lloyd Department of Pathology and Laboratory Medicine, University of Wisconsin School of Medicine and Public Health, Zhejiang, China

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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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Annu Makker Post Graduate Department of Pathology, King George's Medical University, Lucknow 226003, Uttar Pradesh, India

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Madhu Mati Goel Post Graduate Department of Pathology, King George's Medical University, Lucknow 226003, Uttar Pradesh, India

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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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Claire E Fletcher 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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D Alwyn Dart 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
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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Charlotte L Bevan 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

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Zhe Wang Department of Gastroenterology, Tongji Hospital, Tongji University School of Medicine, Shanghai, China
Division of Gastroenterology, Department of Medicine, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA

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Ke Ma Division of Gastroenterology, Department of Medicine, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA

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Steffie Pitts Cellular and Molecular Medicine Graduate Program, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA

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Yulan Cheng Division of Gastroenterology, Department of Medicine, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA

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Xi Liu Department of Pathology, The First Affiliated Hospital of Xi’ an Jiaotong University, Xi’ an, Shaanxi, China

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Xiquan Ke Department of Gastroenterology, The First Affiliated Hospital of Bengbu Medical College, Bengbu, Anhui, China

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Samuel Kovaka Department of Computer Science, Whiting School of Engineering, Johns Hopkins University, Baltimore, Maryland, USA

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Hassan Ashktorab Cancer Center, Howard University School of Medicine, Washington, District of Columbia, USA

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Duane T Smoot Department of Medicine, Meharry Medical College, Nashville, Tennessee, USA

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Michael Schatz Department of Computer Science, Whiting School of Engineering, Johns Hopkins University, Baltimore, Maryland, USA

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Zhirong Wang Department of Gastroenterology, Tongji Hospital, Tongji University School of Medicine, Shanghai, China

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Stephen J Meltzer 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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Sijin Li Department of Thyroid Surgery, the Second Affiliated Hospital, School of Medicine, South China University of Technology, Guangzhou, China

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Zhen Chen Department of Thyroid Surgery, Guangzhou First People’s Hospital, Guangzhou, China

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Mengchu Liu School of Biomedical Sciences and Engineering, South China University of Technology, Guangzhou International Campus, Guangzhou, China

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Liang Li Medical Research Institute, Guangdong Provincial People’s Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, China

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Wensong Cai Department of Thyroid Surgery, Guangzhou First People’s Hospital, Guangzhou, China

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Zhe-Xiong Lian Guangdong Provincial People’s Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, China

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Haixia Guan Department of Endocrinology, Guangdong Provincial People’s Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, China

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Bo Xu Department of Thyroid Surgery, the Second Affiliated Hospital, School of Medicine, South China University of Technology, Guangzhou, China

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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

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W Solarek 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
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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A M Czarnecka 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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B Escudier 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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Z F Bielecka 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
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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F Lian 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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C Szczylik 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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Avaniyapuram Kannan Murugan Division of Molecular Endocrinology, Department of Molecular Oncology, King Faisal Specialist Hospital and Research Center, Riyadh, Saudi Arabia

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Arasambattu Kannan Munirajan Department of Genetics, Dr ALM PG Institute of Basic Medical Sciences, University of Madras, Taramani, Chennai, India

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Ali S Alzahrani Division of Molecular Endocrinology, Department of Molecular Oncology, King Faisal Specialist Hospital and Research Center, Riyadh, Saudi Arabia

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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

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Libero Santarpia 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
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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Milena Nicoloso 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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George A Calin 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

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