SOCS1 favors the epithelial-mesenchymal transition in melanoma, promotes tumor progression and prevents antitumor immunity by PD-L1 expression

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dc.citation.volume7
dc.contributor.authorBerzaghi, R. [UNIFESP]
dc.contributor.authorMaia, V. S. C.
dc.contributor.authorPereira, F. V.
dc.contributor.authorMelo, F. M. [UNIFESP]
dc.contributor.authorGuedes, M. S. [UNIFESP]
dc.contributor.authorOrigassa, C. S. T.
dc.contributor.authorScutti, J. B.
dc.contributor.authorMatsuo, A. L. [UNIFESP]
dc.contributor.authorCamara, N. O. S.
dc.contributor.authorRodrigues, E. G. [UNIFESP]
dc.contributor.authorTravassos, L. R. [UNIFESP]
dc.coverageLondon
dc.date.accessioned2020-07-17T14:03:15Z
dc.date.available2020-07-17T14:03:15Z
dc.date.issued2017
dc.description.abstractSilencing of SOCS1 protein with shRNAi lentivirus (shR-SOCS1) led to partial reversion of the tumorigenic phenotype of B16F10-Nex2 melanoma cells. SOCS1 silencing inhibited cell migration and invasion as well as in vitro growth by cell cycle arrest at S phase with increased cell size and nuclei. Down-regulation of SOCS1 decreased the expression of epidermal growth factor receptor, Ins-R alpha, and fibroblast growth factor receptors. The present work aimed at analyzing the SOCS1 cell signaling and expression of proteins relevant to tumor development. An RNA microarray analysis of B16F10-Nex2 melanoma cells with SOCS1 silenced by shRNAi-SOCS1 was undertaken in comparison with cells transduced with the empty vector. Among 609 differentially expressed genes, c-Kit, Met and EphA3 cytokine/tyrosine-kinase (TK) receptors were down regulated. A significant decrease in the expression of TK receptors, the phosphorylation of mediators of ERK1/2 and p38 pathways and STAT3 (S727) were observed. Subcutaneous immunization with shR-SOCS1-transduced viable tumor cells rendered protection against melanoma in a syngeneic model, with decreased expression of PD-L1 and of matrix metallo-proteinases (MMPs) and CD-10 in those cells. The present work shows the role of SOCS1 in murine melanoma development and the potential of SOCS1-silenced tumor cells in raising an effective anti-melanoma immune response.en
dc.description.affiliationUniv Sao Paulo, Dept Microbiol Immunol & Parasitol, Expt Oncol Unit, Sao Paulo, Brazil
dc.description.affiliationRecepta Biopharma Sao Paulo, Sao Paulo, Brazil
dc.description.affiliationUniv Sao Paulo, Lab Canc Immunobiol, Sao Paulo, Brazil
dc.description.affiliationUniv Fed Sao Paulo, Dept Immunol, Sao Paulo, Brazil
dc.description.affiliationUniv Texas MD Anderson Canc Ctr, Dept Immunol, Immunotherapy Platform, Houston, TX 77030 USA
dc.description.affiliationUniv Fed Sao Paulo, Interdept Grp Hlth Econ Grides, Sao Paulo, SP, Brazil
dc.description.affiliationUniv Sao Paulo, Biomed Sci Inst 4, Immunol Dept, Sao Paulo, Brazil
dc.description.affiliationUnifespUniv Fed Sao Paulo, Dept Immunol, Sao Paulo, Brazil
dc.description.affiliationUnifespUniv Fed Sao Paulo, Interdept Grp Hlth Econ Grides, Sao Paulo, SP, Brazil
dc.description.sourceWeb of Science
dc.description.sponsorshipState of Sao Paulo Foundation for Research Support (FAPESP)
dc.description.sponsorshipBrazilian National Council for Research and Development (CNPq)
dc.description.sponsorshipIDFAPESP: 2010/51423-0
dc.description.sponsorshipIDFAPESP: 2012/17473-6
dc.description.sponsorshipIDCNPq: 157559/2015-7
dc.format.extent-
dc.identifierhttp://dx.doi.org/10.1038/srep40585
dc.identifier.citationScientific Reports. London, v. 7, p. -, 2017.
dc.identifier.doi10.1038/srep40585
dc.identifier.fileWOS000391664900001.pdf
dc.identifier.issn2045-2322
dc.identifier.urihttps://repositorio.unifesp.br/handle/11600/55262
dc.identifier.wosWOS:000391664900001
dc.language.isoeng
dc.publisherNature Publishing Group
dc.relation.ispartofScientific Reports
dc.rightsinfo:eu-repo/semantics/openAccess
dc.titleSOCS1 favors the epithelial-mesenchymal transition in melanoma, promotes tumor progression and prevents antitumor immunity by PD-L1 expressionen
dc.typeinfo:eu-repo/semantics/article
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