Hedgehog signaling pathway mediates tongue tumorigenesis in wild-type mice but not in Ga13-deficient mice

Página do item simplificado
dc.contributorSistema FMUSP-HC: Faculdade de Medicina da Universidade de São Paulo (FMUSP) e Hospital das Clínicas da FMUSP
dc.contributor.authorSANTOS, Debora de Oliveira
dc.contributor.authorLOYOLA, Adriano Mota
dc.contributor.authorCARDOSO, Sergio Vitorino
dc.contributor.authorCHAMMAS, Roger
dc.contributor.authorLIU, Fu-Tong
dc.contributor.authorFARIA, Paulo Rogerio de
dc.date.accessioned2015-04-22T22:08:39Z
dc.date.available2015-04-22T22:08:39Z
dc.date.issued2014
dc.description.abstractOral squamous cell carcinoma (OSCC) is one of the most aggressive cancers of the oral cavity and an important cause of death worldwide. Currently, there are limited clinical tools aiding clinicians to establish its early diagnosis, and genetic and epigenetic events leading to the pathogenesis of OSCC remain unsolved. The use of carcinogen-induced knocked out mouse models would help to improve its early detection and also determine the role of proteins such as galectin-3 (Gal3) in this process. Here we used a mouse model of oral carcinogenesis employing two mouse genotypes: wild-type (Gal3 +/+) and galectin-3-deficient mice (Gal3 -/-) challenged by the carcinogen 4NQO for 16 weeks. After induction, the expression of Wnt1, Wnt3A, Shh and Gli3 proteins in tongue samples was evaluated using an immunohistochemistry approach. All samples of dysplasia and carcinoma were negative for Wnt1. Wnt3A expression was detected in both Gal3 +/+ and Gal3 -/- mice, at similar levels. Wnt3A expression did not predict tongue tumorigenesis in either genotype. Dysplastic- and carcinoma-expressing Shh was statistically significantly higher in Gal3 +/+ mice than Gal3 -/- mice (p < 0.0001), and was associated with tongue tumorigenesis only in the former. Gli3 expression decreased and increased from dysplasia to carcinoma in Gal3 +/+ and Gal3 -/- mice, respectively, although the difference was not significant. The results suggest that activated Wnt signaling is present in both mice, and that the Hh signaling pathway might play a role in tongue carcinoma development in Gal3 +/+ mice.
dc.description.indexMEDLINE
dc.description.sponsorshipResearch Supporting Foundation of Minas Gerais [FAPEMIG-CDS-APQ-00397-09]
dc.identifier.citationEXPERIMENTAL AND MOLECULAR PATHOLOGY, v.97, n.3, p.332-337, 2014
dc.identifier.doi10.1016/j.yexmp.2014.09.018
dc.identifier.eissn1096-0945
dc.identifier.issn0014-4800
dc.identifier.urihttps://observatorio.fm.usp.br/handle/OPI/8953
dc.language.isoeng
dc.publisherACADEMIC PRESS INC ELSEVIER SCIENCE
dc.relation.ispartofExperimental and Molecular Pathology
dc.rightsrestrictedAccess
dc.rights.holderCopyright ACADEMIC PRESS INC ELSEVIER SCIENCE
dc.subjectOral carcinogenesis
dc.subjectGalectin-3
dc.subjectTongue
dc.subjectMice
dc.subjectSonic hedgehog
dc.subjectWnt signaling
dc.subject.othersquamous-cell carcinoma
dc.subject.othersonic hedgehog
dc.subject.otherbeta-catenin
dc.subject.othertargeted disruption
dc.subject.otheroral carcinogenesis
dc.subject.othernegative regulator
dc.subject.othergalectin-3
dc.subject.othercancer
dc.subject.otherexpression
dc.subject.otherprogression
dc.subject.wosPathology
dc.titleHedgehog signaling pathway mediates tongue tumorigenesis in wild-type mice but not in Ga13-deficient mice
dc.typearticle
dc.type.categoryoriginal article
dc.type.versionpublishedVersion
dspace.entity.typePublication
hcfmusp.affiliation.countryEstados Unidos
hcfmusp.affiliation.countryisous
hcfmusp.author.externalSANTOS, Debora de Oliveira:Univ Fed Uberlandia, Inst Biomed Sci, Dept Morphol, BR-38405320 Uberlandia, MG, Brazil
hcfmusp.author.externalLOYOLA, Adriano Mota:Univ Fed Uberlandia, Sch Dent, BR-38405320 Uberlandia, MG, Brazil
hcfmusp.author.externalCARDOSO, Sergio Vitorino:Univ Fed Uberlandia, Sch Dent, BR-38405320 Uberlandia, MG, Brazil
hcfmusp.author.externalLIU, Fu-Tong:Univ Calif Davis, Sch Med, Dept Dermatol, Sacramento, CA 95817 USA
hcfmusp.author.externalFARIA, Paulo Rogerio de:Univ Fed Uberlandia, Inst Biomed Sci, Dept Morphol, BR-38405320 Uberlandia, MG, Brazil
hcfmusp.citation.scopus4
hcfmusp.contributor.author-fmusphcROGER CHAMMAS
hcfmusp.description.beginpage332
hcfmusp.description.endpage337
hcfmusp.description.issue3
hcfmusp.description.volume97
hcfmusp.origemWOS
hcfmusp.origem.scopus2-s2.0-84907560504
hcfmusp.origem.wosWOS:000346685700003
hcfmusp.publisher.citySAN DIEGO
hcfmusp.publisher.countryUSA
hcfmusp.relation.referenceAbdel-Aziz HO, 2008, J CANCER RES CLIN, V134, P777, DOI 10.1007/s00432-007-0345-3
hcfmusp.relation.referenceAmakye D, 2013, NAT MED, V19, P1410, DOI 10.1038/nm.3389
hcfmusp.relation.referenceBeachy PA, 2004, NATURE, V432, P324, DOI 10.1038/nature03100
hcfmusp.relation.referenceBerman DM, 2003, NATURE, V425, P846, DOI 10.1038/nature01972
hcfmusp.relation.referenceBriscoe J, 2013, NAT REV MOL CELL BIO, V14, P416, DOI 10.1038/nrm3598
hcfmusp.relation.referenceCardesa A., 2005, WHO CLASSIFICATION T, P118
hcfmusp.relation.referenceda Silva SD, 2011, ORAL ONCOL, V47, P783, DOI 10.1016/j.oraloncology.2011.07.004
hcfmusp.relation.referencede Faria PR, 2011, EXP MOL PATHOL, V90, P189, DOI 10.1016/j.yexmp.2010.12.007
hcfmusp.relation.referenceDimitrova K, 2013, ONKOLOGIE, V36, P279, DOI 10.1159/000350322
hcfmusp.relation.referenceEude-Le Parco I, 2009, GLYCOBIOLOGY, V19, P68, DOI 10.1093/glycob/cwn105
hcfmusp.relation.referenceFracalossi ACC, 2010, EXP MOL PATHOL, V88, P176, DOI 10.1016/j.yexmp.2009.11.004
hcfmusp.relation.referenceGiles RH, 2003, BBA-REV CANCER, V1653, P1, DOI 10.1016/S0304-419X(03)00005-2
hcfmusp.relation.referenceHagen T, 2002, BIOCHEM BIOPH RES CO, V294, P324, DOI 10.1016/S0006-291X(02)00485-0
hcfmusp.relation.referenceHonami T, 2012, ORAL ONCOL, V48, P49, DOI 10.1016/j.oraloncology.2011.08.026
hcfmusp.relation.referenceHsu DK, 2000, AM J PATHOL, V156, P1073, DOI 10.1016/S0002-9440(10)64975-9
hcfmusp.relation.referenceIshida K, 2007, MOL CANCER, V9, P6
hcfmusp.relation.referenceKanojia D, 2006, ORAL ONCOL, V42, P655, DOI 10.1016/j.oraloncology.2005.10.013
hcfmusp.relation.referenceKise Y, 2009, BIOCHEM BIOPH RES CO, V387, P569, DOI 10.1016/j.bbrc.2009.07.087
hcfmusp.relation.referenceLiu FT, 2005, NAT REV CANCER, V5, P29, DOI 10.1038/nrc1527
hcfmusp.relation.referenceLUMERMAN H, 1995, ORAL SURG ORAL MED O, V79, P321, DOI 10.1016/S1079-2104(05)80226-4
hcfmusp.relation.referenceMarkowska AI, 2010, J EXP MED, V207, P1981, DOI 10.1084/jem.20090121
hcfmusp.relation.referenceMendonca DF, 2012, INT J CLIN EXP PATHO, V5, P547
hcfmusp.relation.referenceMill P, 2005, DEV CELL, V9, P293, DOI 10.1016/j.devcel.2005.06.009
hcfmusp.relation.referenceMimeault M, 2010, PHARMACOL REV, V62, P497, DOI 10.1124/pr.109.002329
hcfmusp.relation.referenceNishimaki H, 2004, BIOCHEM BIOPH RES CO, V314, P313, DOI 10.1016/j.bbrc.2003.12.097
hcfmusp.relation.referencePaces-Fessy M, 2004, BIOCHEM J, V378, P353, DOI 10.1042/BJ20030786
hcfmusp.relation.referencePerez-Sayans M, 2012, ORAL ONCOL, V48, P56, DOI 10.1016/j.oraloncology.2011.09.001
hcfmusp.relation.referenceReibel J, 2003, CRIT REV ORAL BIOL M, V14, P47
hcfmusp.relation.referenceRuiz I, 1999, TRENDS GENET, V15, P418
hcfmusp.relation.referenceSant'Ana JMDA, 2011, ANTICANCER RES, V31, P2805
hcfmusp.relation.referenceSchneider FT, 2010, AM J PATHOL, V177, P404, DOI 10.2353/ajpath.2010.091079
hcfmusp.relation.referenceShimura T, 2005, CANCER RES, V65, P3535, DOI 10.1158/0008-5472.CAN-05-0104
hcfmusp.relation.referenceShimura T, 2004, CANCER RES, V64, P6363, DOI 10.1158/0008-5472.CAN-04-1816
hcfmusp.relation.referenceSINICROPE FA, 1995, CANCER RES, V55, P237
hcfmusp.relation.referenceSong SM, 2009, CANCER RES, V69, P1343, DOI 10.1158/0008-5472.CAN-08-4153
hcfmusp.relation.referenceTakenaka Yukinori, 2004, Glycoconjugate Journal, V19, P543
hcfmusp.relation.referenceTang JY, 2007, TOXICOL APPL PHARM, V224, P257, DOI 10.1016/j.taap.2006.12.011
hcfmusp.relation.referenceTang XH, 2004, CLIN CANCER RES, V10, P301, DOI 10.1158/1078-0432.CCR-0999-3
hcfmusp.relation.referenceTempe D, 2006, MOL CELL BIOL, V26, P4316, DOI 10.1128/MCB.02183-05
hcfmusp.relation.referenceWang LH, 2006, MODERN PATHOL, V19, P675, DOI 10.1038/modpathol.3800573
hcfmusp.relation.referenceWang YF, 2012, HEAD NECK-J SCI SPEC, V34, P1556, DOI 10.1002/hed.21958
hcfmusp.relation.referenceWatkins D Neil, 2003, Cell Cycle, V2, P196
hcfmusp.relation.referenceXuan YH, 2006, MODERN PATHOL, V19, P1139, DOI 10.1038/modpathol.3800600
hcfmusp.scopus.lastupdate2024-05-10
relation.isAuthorOfPublication1fdeabdc-849e-48e4-ba52-1c124a06b220
relation.isAuthorOfPublication.latestForDiscovery1fdeabdc-849e-48e4-ba52-1c124a06b220
Arquivos
Pacote Original
Agora exibindo 1 - 1 de 1
Nenhuma Miniatura disponível
Nome:
art_SANTOS_Hedgehog_signaling_pathway_mediates_tongue_tumorigenesis_in_wildtype_2014.PDF
Tamanho:
1.1 MB
Formato:
Adobe Portable Document Format
Descrição:
publishedVersion (English)
Baixar
Coleções
Artigos e Materiais de Revistas Científicas - FM/MDR
Artigos e Materiais de Revistas Científicas - LIM/24
Artigos e Materiais de Revistas Científicas - ODS/03