Arginase 2 and nitric oxide synthase: Pathways associated with the pathogenesis of thyroid tumors

Página do item simplificado
dc.contributor.authorSousa, Maria Sharmila A. [UNIFESP]
dc.contributor.authorLatini, Flavia R. M. [UNIFESP]
dc.contributor.authorMonteiro, Hugo P. [UNIFESP]
dc.contributor.authorCerutti, Janete M. [UNIFESP]
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.date.accessioned2016-01-24T14:05:28Z
dc.date.available2016-01-24T14:05:28Z
dc.date.issued2010-09-15
dc.description.abstractWe have previously shown that ARG2 expression was increased in most malignant thyroid tumors, but absent in benign lesions and normal tissues. Small interfering RNA knockdown was used to investigate the role of ARG2 in a thyroid carcinoma cell line. ARG2 knockdown decreased eNOS expression as well as the expression of eNOS-related genes (p21, Akt1, HIF-1, VEGF, and CAVI). ARG2 silencing changed tumor properties of thyroid cancer cells promoting apoptosis and reduced expression of cell proliferation markers. These results, coupled with enhanced nitric oxide production and elevated reactive oxygen species (ROS) levels, account for the altered intracellular redox environment. Genes related to either production (DUOX1 and NOX4) or catabolism (SODS) of ROS and reactive nitrogen species were negatively modulated by ARG2 knockdown. Additionally, a positive correlation of ARG2 with eNOS and related genes was investigated in thyroid tumors, further substantiating our in vitro findings. Our results suggest that ARG2 and eNOS may work in a coordinated manner and the underlying mechanism might be of major significance for thyroid tumorigenesis and/or tumor progression pathways. Fine modulation of ARG2, eNOS, and related genes may represent a potential source for targeted therapy of several cancer types. (C) 2010 Elsevier Inc. All rights reserved.en
dc.description.affiliationUniversidade Federal de São Paulo, Genet Basis Thyroid Tumors Lab, Div Genet, Dept Morphol & Genet, BR-04039032 São Paulo, Brazil
dc.description.affiliationUniversidade Federal de São Paulo, Div Endocrinol, Dept Med, BR-04039032 São Paulo, Brazil
dc.description.affiliationUniversidade Federal de São Paulo, Interdisciplinary Ctr Gene Therapy, Dept Biochem, BR-04039032 São Paulo, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Genet Basis Thyroid Tumors Lab, Div Genet, Dept Morphol & Genet, BR-04039032 São Paulo, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Div Endocrinol, Dept Med, BR-04039032 São Paulo, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Interdisciplinary Ctr Gene Therapy, Dept Biochem, BR-04039032 São Paulo, Brazil
dc.description.sourceWeb of Science
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.description.sponsorshipIDFAPESP: 05/60330-8
dc.description.sponsorshipIDFAPESP: 09/11257-7
dc.format.extent997-1007
dc.identifierhttp://dx.doi.org/10.1016/j.freeradbiomed.2010.06.006
dc.identifier.citationFree Radical Biology and Medicine. New York: Elsevier B.V., v. 49, n. 6, p. 997-1007, 2010.
dc.identifier.doi10.1016/j.freeradbiomed.2010.06.006
dc.identifier.issn0891-5849
dc.identifier.urihttp://repositorio.unifesp.br/handle/11600/32911
dc.identifier.wosWOS:000281047000006
dc.language.isoeng
dc.publisherElsevier B.V.
dc.relation.ispartofFree Radical Biology and Medicine
dc.rightsinfo:eu-repo/semantics/restrictedAccess
dc.rights.licensehttp://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dc.subjectARG2en
dc.subjecteNOSen
dc.subjectThyroid carcinomaen
dc.subjectNOen
dc.subjectROSen
dc.subjectApoptosisen
dc.subjectFree radicalsen
dc.titleArginase 2 and nitric oxide synthase: Pathways associated with the pathogenesis of thyroid tumorsen
dc.typeinfo:eu-repo/semantics/article
Arquivos
Coleções
Em verificação - Geral