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. Drug treatments and cell proliferation assay The CDK4/6 inhibitor palbociclib was provided by Pfizer and prepared in 50 mM lactate. The PI3K/mTOR inhibitor, omipalisib, and the MEK inhibitor, trametinib, were purchased from Selleck Chemicals (Houston
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with metastatic CRPC, the survival rate of patients with metastatic CRPC remains poor and additional therapeutic approaches are needed. The phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) pathway is a key oncogenic
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( Table 2 ). Table 2 Primary antibodies used in this study. Proteins Primary antibodies Details TAGLN2 Rabbit polyclonal anti-TAGLN2 antibody 1:1000, 10234-2-AP, Proteintech t-PI3K Mouse monoclonal anti-PI3K p85
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transduced by Janus activated kinase/signal transducers and activators of transcription (JAK/STAT), mitogen-activated protein kinase (MAPK), and phosphatidylinisitol-3′-kinase (PI3K) signaling pathways ( Hegyi et al . 2004 ). Previously, we have shown that
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German Center for Diabetes Research (DZD), Neuherberg, Germany
Technische Universität München, Chair of Experimental Genetics, Freising, Germany
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( Eisenhofer et al. 2011 ). Activation of the PI3K/AKT/mTOR pathway plays a pivotal role in the initiation and progression of many human malignancies by enhancing cell survival, stimulating cell proliferation and inhibiting apoptosis ( Cantrell 2001
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University of the Chinese Academy of Sciences, Beijing, China
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overexpressed in pNEN tissues and was positively correlated with H19 expression to promote cancer progression. Moreover, higher VGF expression was markedly related to poor differentiation and advanced stage. RNA sequence analysis revealed that H19 activates PI3K
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Section of Endocrinology, Laboratorio in Rete del Tecnopolo ‘Tecnologie delle Terapie Avanzate’ (LTTA), Department of Cardiological, Department of Morphology, Department of Medical Sciences, University of Ferrara, Via Savonarola 9, 44121 Ferrara, Italy
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Section of Endocrinology, Laboratorio in Rete del Tecnopolo ‘Tecnologie delle Terapie Avanzate’ (LTTA), Department of Cardiological, Department of Morphology, Department of Medical Sciences, University of Ferrara, Via Savonarola 9, 44121 Ferrara, Italy
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Section of Endocrinology, Laboratorio in Rete del Tecnopolo ‘Tecnologie delle Terapie Avanzate’ (LTTA), Department of Cardiological, Department of Morphology, Department of Medical Sciences, University of Ferrara, Via Savonarola 9, 44121 Ferrara, Italy
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-BEZ235. The latter is an imidazo (4,5-c)quinoline derivative that inhibits both phosphatidylinositol 3-kinase (PI3K) and mTOR activities, inducing G1 arrest in cell-cycle progression ( Maira et al . 2008 ). It has been demonstrated previously that NVP
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Division of Reproductive Science in Medicine, Department of Obstetrics and Gynecology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA
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-significant; * P < 0.1; ** P < 0.05; and *** P < 0.01. NH, no hormone; PDX, patient-derived xenograft; SMC, smooth muscle cells. A full color version of this figure is available at https://doi.org/10.1530/ERC-18-0184 . Regulation of MAPK and PI3K
Translational Research, Academic Biochemistry, Royal Marsden Hospital, Molecular Pathology, Department of Biomedical Sciences and Human Oncology, Roche Diagnostics GmbH, Breast Unit, The Breakthrough Breast Cancer Research Centre, London, UK
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Translational Research, Academic Biochemistry, Royal Marsden Hospital, Molecular Pathology, Department of Biomedical Sciences and Human Oncology, Roche Diagnostics GmbH, Breast Unit, The Breakthrough Breast Cancer Research Centre, London, UK
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Translational Research, Academic Biochemistry, Royal Marsden Hospital, Molecular Pathology, Department of Biomedical Sciences and Human Oncology, Roche Diagnostics GmbH, Breast Unit, The Breakthrough Breast Cancer Research Centre, London, UK
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-IGF1R phosphorylating IRS1, IRS2 and Shc, activating transduction pathways such as PI3K and Ras/Raf/MAPK ( Riedemann & Macaulay 2006 ). In addition, IGF1R physically associates with ERα and this leads to activation of IGF1R and the downstream ERK1
Barts and the London School of Medicine, Department of Endocrinology and Internal Medicine, Division of Endocrinology and Metabolism, Internal Medicine, Institute of Endocrinology and Metabolism, Centre for Endocrinology, London, UK
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Barts and the London School of Medicine, Department of Endocrinology and Internal Medicine, Division of Endocrinology and Metabolism, Internal Medicine, Institute of Endocrinology and Metabolism, Centre for Endocrinology, London, UK
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Barts and the London School of Medicine, Department of Endocrinology and Internal Medicine, Division of Endocrinology and Metabolism, Internal Medicine, Institute of Endocrinology and Metabolism, Centre for Endocrinology, London, UK
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identified ( Dworakowska & Grossman 2009 b ). Two major signalling pathways responsible for regulating cell growth and proliferation, downstream of growth factor receptors, are the phosphatidylinositol 3-kinase (PI3K)/Akt and Raf/mitogen-activated protein