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Silencing of NAMPT leads to up-regulation of insulin receptor substrate 1 gene expression in U87 glioma cells

Abstract

Objective. The aim of the present study was to investigate the effect of adipokine NAMPT (nicotinamide phosphoribosyltransferase) silencing on the expression of genes encoding IRS1 (insulin receptor substrate 1) and some other proliferation related proteins in U87 glioma cells for evaluation of the possible significance of this adipokine in intergenic interactions.

Methods. The silencing of NAMPT mRNA was introduced by NAMPT specific siRNA. The expression level of NAMPT, IGFBP3, IRS1, HK2, PER2, CLU, BNIP3, TPD52, GADD45A, and MKI67 genes was studied in U87 glioma cells by quantitative polymerase chain reaction. Anti-visfatin antibody was used for detection of NAMPT protein by Western-blot analysis.

Results. It was shown that the silencing of NAMPT mRNA led to a strong down-regulation of NAMPT protein and significant modification of the expression of IRS1, IGFBP3, CLU, HK2, BNIP3, and MKI67 genes in glioma cells and a strong up-regulation of IGFBP3 and IRS1 and down-regulation of CLU, BNIP3, HK2, and MKI67 gene expressions. At the same time, no significant changes were detected in the expression of GADD45A, PER2, and TPD52 genes in glioma cells treated by siRNA specific to NAMPT. Furthermore, the silencing of NAMPT mRNA suppressed the glioma cell proliferation.

Conclusions. Results of this investigation demonstrated that silencing of NAMPT mRNA with corresponding down-regulation of NAMPT protein and suppression of the glioma cell proliferation affected the expression of IRS1 gene as well as many other genes encoding the proliferation related proteins. It is possible that dysregulation of most of the studied genes in glioma cells after silencing of NAMPT is reflected by a complex of intergenic interactions and that NAMPT is an important factor for genome stability and regulatory mechanisms contributing to the control of glioma cell metabolism and proliferation.

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Genetic and epigenetic differences of benign and malignant pheochromocytomas and paragangliomas (PPGLs)

Abstract

Pheochromocytomas and paragangliomas (PPGLs) are tumors arising from the adrenal medulla and sympathetic/parasympathetic paraganglia, respectively. According to Th e Cancer Genome Atlas (TCGA), approximately 40% of PPGLs are due to germ line mutations in one of 16 susceptibility genes, and a further 30% are due to somatic alterations in at least seven main genes (VHL, EPAS1, CSDE1, MAX, HRAS, NF1, RET, and possibly KIF1B). Th e diagnosis of malignant PPGL was straight forward in most cases as it was defined as presence of PPGL in non-chromaffin tissues. Accordingly, there is an extreme need for new diagnostic marker(s) to identify tumors with malignant prospective. Th e aim of this study was to review all suggested genetic and epigenetic alterations that are remarkably different between benign and malignant PPGLs. It seems that more than two genetic mutation clusters in PPGLs and other genetic and methylation biomarkers could be targeted for malignancy discrimination in different studies.

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Mutations in SURF1 are important genetic causes of Leigh syndrome in Slovak patients

syndrome. Biochem Biophys Res Commun 497, 1043–1048, 2018. Martinelli D, Catteruccia M, Piemonte F, Pastore A, Tozzi G, Dionisi-Vici C, Pontrelli G, Corsetti T, Livadiotti S, Kheifets V, Hinman A, Shrader WD, Thoolen M, Klein MB, Bertini E, Miller G. EPI-743 reverses the progression of the pediatric mitochondrial disease-genetically defined Leigh Syndrome. Mol Genet Metab 107, 383–388, 2012. McLaren W, Gil L, Hunt SE, Riat HS, Ritchie GR, Thormann A, Flicek P, Cunningham F. The Ensembl Variant Effect Predictor. Genome Biol 17, 122, 2016. Paila U

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Lack of association between TCF7L2 gene variants and type 2 diabetes mellitus in a Brazilian sample of patients with the risk for cardiovascular disease

. Glucagon-like peptide-1 activation of TCF7L2-dependent Wnt signaling enhances pancreatic beta cell proliferation. J Biol Chem 283, 8723–8735, 2008. Long J, Edwards T, Signorello LB, Cai Q, Zheng W, Shu XO, Blot WJ. Evaluation of genome-wide association study-identified type 2 diabetes loci in African Americans. Am J Epidemiol 176, 995–1001, 2012. Lyssenko V, Lupi R, Marchetti P, Del Guerra S, Orho-Melander M, Almgren P, Sjogren M, Ling C, Eriksson KF, Lethagen AL, Mancarella R, Berglund G, Tuomi T, Nilsson P, Del Prato S, Groop L. Mechanisms by which common

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The expression of Drosha, DGCR8, Dicer and Ago-2 genes are upregulated in human umbilical vein endothelial cells under hyperglycemic condition

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Novel insights into genetics and clinics of the HNF1A-MODY

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Exposure to a single immobilization or lipopolysaccharide challenge increases expression of genes implicated in the development of Alzheimer’s disease in the mice brain cortex

, Prescott SM, McIntyre TM. Retrograde inflammatory signaling from neutrophils to endothelial cells by soluble interleukin-6 receptor alpha. J Clin Invest 100, 2752–2756, 1997. Moraes CF, Lins TC, Carmargos EF, Naves JO, Pereira RW, Nobrega OT. Lessons from genome-wide association studies findings in Alzheimer’s disease. Psychogeriatrics 12, 62–73, 2012. Muller UC, Deller T, Korte M. Not just amyloid: physiological functions of the amyloid precursor protein family. Nat Rev Neurosci 18, 281–298, 2017. Murakami N, Yamaki T, Iwamoto Y, Sakakibara T, Kobori N

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Progress in micro RNA focused research in endocrinology

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Pheochromocytoma

, Jefferys SR, de Cubas AA, Wenz B, Korpershoek E, Amelio AL, Makowski L, Rathmell WK, Gimenez-Roqueplo AP, Giordano TJ, Asa SL, Tischler AS; Cancer Genome Atlas Research Network, Pacak K, Nathanson KL, Wilkerson MD. Comprehensive molecular characterization of pheochromocytoma and paraganglioma. Cancer Cell 31, 181–193, 2017. Flynn A, Benn D, Clifton-Bligh R, Robinson B, Trainer AH, James P, Hogg A, Waldeck K, George J, Li J, Fox SB, Gill AJ, McArthur G, Hicks RJ, Tothill RW. The genomic landscape of phaeochromocytoma. J Pathol 236, 78–89, 2015. Francis IR

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Multiple functions and essential roles of nuclear receptor coactivators of bHLH-PAS family

, Istomin AY, Livesay DR, Jacobs DJ, Swerdloff RS, Miksovska J, Larsen RW, Bhasin S. Kinetic and thermodynamic characterization of dihydrotestosterone-induced conformational perturbations in androgen receptor ligand-binding domain. Mol Endocrinol 23, 1231-1241, 2009. Jones S. An overview of the basic helix-loop-helix proteins. Genome Biol 5, 226, 2004. Jung SY, Malovannaya A, Wei J, O’Malley BW, Qin J. Proteomic analysis of steady-state nuclear hormone receptor coactivator complexes. Mol Endocrinol 19, 2451-2465, 2005

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