Please use this identifier to cite or link to this item: https://repositorio.unifesp.br/handle/11600/55262
Title: SOCS1 favors the epithelial-mesenchymal transition in melanoma, promotes tumor progression and prevents antitumor immunity by PD-L1 expression
Authors: Berzaghi, R. [UNIFESP]
Maia, V. S. C.
Pereira, F. V.
Melo, F. M. [UNIFESP]
Guedes, M. S. [UNIFESP]
Origassa, C. S. T.
Scutti, J. B.
Matsuo, A. L. [UNIFESP]
Camara, N. O. S.
Rodrigues, E. G. [UNIFESP]
Travassos, L. R. [UNIFESP]
Issue Date: 2017
Publisher: Nature Publishing Group
Citation: Scientific Reports. London, v. 7, p. -, 2017.
Abstract: Silencing 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.
URI: https://repositorio.unifesp.br/handle/11600/55262
ISSN: 2045-2322
Other Identifiers: http://dx.doi.org/10.1038/srep40585
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