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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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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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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serum (FB) (Natocor, Córdoba, Argentina) and penicillin 100 units/mL-streptomycin 100 µg/mL (Gibco) in a humidified 5% CO 2 atmosphere at 37°C. In this study, cell migration was characterized by the rhodamine-conjugated phalloidin staining of cell
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properties ( 4 ). Vasoinhibins (Vi) are generated by proteolytic cleavage within the long-loop structure connecting the third helix and the fourth helix of PRL ( 5 ). Vi can act on endothelial cells to induce apoptosis and inhibit proliferation and migration
James P. Wilmot Cancer Institute, University of Rochester Medical Center, Rochester, New York, USA
Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
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
Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
James Buchanan Brady Urological Institute, Johns Hopkins University School of Medicine, Baltimore, Maryland, 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 P. Wilmot Cancer Institute, University of Rochester Medical Center, Rochester, New York, 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
Department of Pathology, University of Alabama at Birmingham, Birmingham, Alabama, USA
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James P. Wilmot Cancer Institute, University of Rochester Medical Center, Rochester, New York, USA
Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
James Buchanan Brady Urological Institute, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
Department of Urology, University of Rochester Medical Center, Rochester, New York, USA
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functional role of ATF2 in cell proliferation, migration and invasion of bladder cancer, an ATF2-shRNA was stably expressed in AR-positive and AR-negative bladder cancer lines where ATF2 knockdown did not significantly affect AR expression ( Fig. 2A ). We
Universitat Oberta Catalunya (UOC), Barcelona, Spain
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Univ Autònoma de Barcelona, Cerdanyola del Vallès, Spain
Fundació Institut d’Investigació en Ciències de la Salut Germans Trias i Pujol, Barcelona, Spain
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Univ Autònoma de Barcelona, Cerdanyola del Vallès, Spain
Fundació Institut d’Investigació en Ciències de la Salut Germans Trias i Pujol, Barcelona, Spain
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spinal ependymal precursors) ( 12 ). GH was shown to stimulate proliferation, differentiation, migration and survival of astrocytes and oligodendrocytes in animal models. This could be in part because of a GH-mediated neuronal anti-apoptotic effect (Akt
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Background: Transforming growth factor beta receptor III (TGFBR3) has been shown to play a tumor suppressive role in a variety of cancers. However, its role in papillary thyroid cancer (PTC) remains unknown.
Method: TGFBR3 expression levels in PTC were analyzed utilizing TCGA and GEO database. Edu, wounding healing and Transwell assays were used to evaluate cell proliferation, migration and invasion. Transcriptome sequencing, qRT-PCR and Western blotting were used to detect the underlying mechanism of TGFBR3 in PTC progression.
Result: This study demonstrated that TGFBR3 expression was significantly down-regulated in PTC compared to normal thyroid tissues. Low expression of TGFBR3 was associated with poor prognosis of patients with PTC. Furthermore, TGFBR3 expression positively correlated with thyroid differentiation score. In investigating the biological impact of TGFBR3 over-expression in PTC cell lines, we found that the proliferation, migration and invasion of PTC cells were significantly inhibited in response to TGFBR3 overexpression. Moreover, we also demonstrated that overexpression of TGFBR3 inhibited PI3K/AKT pathway and epithelial mesenchymal transformation processes. Lastly, TGFBR3 expression was found to be involved in tumor immune infiltration, highlighting its potential influence on immune dynamics within the tumor microenvironment in PTC.
Conclusion: TGFBR3 plays a tumor suppressive role in PTC progression by inhibiting PI3K/AKT pathway and EMT.
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Background: Collagen type VIII α 1 chain (COL8A1), a collagen type VIII protein, has been suggested to exert various functions in progression of multiple cancers. However, the effect of COL8A1 in papillary thyroid cancer (PTC) has not been elucidated.
Methods: The Cancer Genome Atlas (TCGA) databases were applied to investigate the COL8A1 expression and its clinical significance in PTC. The COL8A1 expression level was further validated using Gene Expression Omnibus (GEO) data and clinical paired PTC tissues. Additionally, Kaplan-Meier curve was used to analyze the prognosis. The cell migrative and invasive abilities were evaluated by wound healing assay and Transwell assay. CCK8 assays were used to evaluate proliferation of PTC cells. Western blotting was conducted to explore the potential mechanisms involved in the pro-tumor role of COL8A1. The correlation between immune cell infiltration and COL8A1 was analyzed using Tumor Immune Estimation Resource (TIMER) database and the single-sample GSEA (ssGSEA) method.
Results: We found that COL8A1 was upregulated in PTC (P<0.05). High COL8A1 expression level was significantly associated with advanced T stage (P<0.01), N stage (P<0.001) and poor prognosis (P=0.0142) in PTC. Furthermore, cell migration and invasion were significantly reduced following COL8A1 knockdown (P<0.001). Mechanistic studies demonstrated that the epithelial-to-mesenchymal transition (EMT) related proteins (FN1, MMP9, MMP7, ZEB2 and Twist1) and phosphorylation of AKT and ERK were obviously down-regulated after COL8A1 knockdown (P<0.01). Moreover, COL8A1 expression was correlated with immune cell infiltration.
Conclusion: Our study demonstrates that COL8A1 may function as an oncogene and a potential prognostic biomarker for PTC patients.
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Universidade de São Paulo, Zebrafish Facility, São Paulo, São Paulo, Brazil
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of neural progenitor cells, in the formation of the neural tube, in neuronal migration and in axon elongation ( 25 , 26 , 27 , 28 , 29 , 30 ). Consistent with these pleiotropic functions, abnormalities in critical domains of N-cadherin have been
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EHESP-School of Public Health, Rennes, France
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Inserm (Institut National de la Santé et de la Recherche Médicale), Irset – Inserm, UMR 1085, Rennes, France
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particular sensitivity for disruption occurring both prenatally and postnatally: (i) mitosis and migration of primordial germ cells (PGC); (ii) meiosis and sex differentiation (iii) germ cell nest breakdown and follicle assembly and (iv) follicle recruitment
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neurons is accompanied by the development and/or migration of the olfactory system in the early fetus, patients with Kallmann syndrome (KS) manifest a combined dysfunction of the GnRH and olfactory systems ( 2 ). IGD is also associated with a normal sense
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, more evidence demonstrates estrogen could influence cell proliferation and migration elicited by combining steroid hormone receptors such as G protein-coupled estrogen receptor 1 (GPER), ERβ or estrogen-related receptors ( 7 , 8 , 9 , 10 ). GPER