Mutual paracrine effects of oral squamous cell carcinoma cells and normal oral fibroblasts: Induction of fibroblast to myofibroblast transdifferentiation and modulation of tumor cell proliferation

dc.creatorKellermann, MG
dc.creatorSobral, LM
dc.creatorda Silva, SD
dc.creatorZecchin, KG
dc.creatorGraner, E
dc.creatorLopes, MA
dc.creatorKowalski, LP
dc.creatorColetta, RD
dc.date2008
dc.dateMAY
dc.date2014-11-14T17:03:39Z
dc.date2015-11-26T17:16:00Z
dc.date2014-11-14T17:03:39Z
dc.date2015-11-26T17:16:00Z
dc.date.accessioned2018-03-29T00:04:13Z
dc.date.available2018-03-29T00:04:13Z
dc.identifierOral Oncology. Elsevier Science Bv, v. 44, n. 5, n. 509, n. 517, 2008.
dc.identifier1368-8375
dc.identifierWOS:000256331800014
dc.identifier10.1016/j.oraloncology.2007.07.001
dc.identifierhttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/81921
dc.identifierhttp://www.repositorio.unicamp.br/handle/REPOSIP/81921
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/81921
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1282181
dc.descriptionSeveral tines of evidence demonstrated that the stroma surrounding the tumors plays an important rote in the growth and progression of several neoplasms, including oral squamous cell carcinomas (OSCC). We evaluated the presence of myofibroblasts in OSCC and determined whether their presence is associated with clinicopathological features of the tumors. We also investigated the mutual paracrine effects of tumor cells and myofibroblasts on fibroblast-myofibroblast transdifferentiation and tumor cell, proliferation. Immunohistochemical analysis showed the similar to 60% of the OSCCs contained myofibroblasts in the stroma of the tumor. Abundant presence of myofibroblasts significantly correlated with N stage, disease stage, regional recurrence, and proliferative potential. of the tumor cells. Using OSCC cell tines and primary oral, normal fibroblasts (ONF), we demonstrated that tumor cells induced transdifferentiation of ONFs to myofibroblasts via secretion of transforming growth factor-betal (TGF-beta 1). In turn, myofibroblasts secreted factors that stimulated OSCC cell proliferation, as revealed by measuring BrdU incorporation and Ki67 expression. The results of the study suggest that during tumor invasion OSCC-derived TGF beta 1 promote fibroblast-myofibroblast transdifferentiation, and that tumor cellular proliferation can be induced by factors released from myofibroblasts, which may favor tumor growth. (c) 2007 Etsevier Ltd. All rights reserved.
dc.description44
dc.description5
dc.description509
dc.description517
dc.languageen
dc.publisherElsevier Science Bv
dc.publisherAmsterdam
dc.publisherHolanda
dc.relationOral Oncology
dc.relationOral Oncol.
dc.rightsfechado
dc.rightshttp://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dc.sourceWeb of Science
dc.subjectoral squamous cell carcinoma
dc.subjectmyofibroblast
dc.subjectsmooth muscle isoform of alpha-actin
dc.subjectclinicopathological correlation
dc.subjectTransforming growth factor-beta1
dc.subjectproliferation
dc.subjectHereditary Gingival Fibromatosis
dc.subjectActivator Upa Production
dc.subjectHuman Prostate-cancer
dc.subjectExtracellular-matrix
dc.subjectStromal Cells
dc.subjectPrognostic-significance
dc.subjectColon-cancer
dc.subjectIn-vitro
dc.subjectExpression
dc.subjectBreast
dc.titleMutual paracrine effects of oral squamous cell carcinoma cells and normal oral fibroblasts: Induction of fibroblast to myofibroblast transdifferentiation and modulation of tumor cell proliferation
dc.typeArtículos de revistas


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