Silencing of claudin-10 expression on B-1 cells impaired the increased metastatic behavior of melanoma cells an in vitro coculture system

Event Abstract Back to Event Silencing of claudin-10 expression on B-1 cells impaired the increased metastatic behavior of melanoma cells an in vitro coculture system Elizabeth C. Perez1, 2*, Patricia Xander1, Maria F. Laurindo1, Ronni R. EBrito3, Bruno Vivanco1, Lika Osugui1, Mario Mariano1 and José D. Lopes1 1 Universisade Federal de São Paulo, Brazil 2 Universidade Paulista, Brazil 3 Centro Universitário São Camilo, Brazil Recent studies in mice are beginning to reveal important immune –modulating functions of B-1 cells, a subset of B cells found predominantly in pleural and peritoneal cavities. Using an in vitro heterotypic coculture system we previously demonstrated that cocultivation of B16 melanoma cells with B-1 cells from C57BL/6 mice (wt), but not with C57BL/6 IL-10 knockout B-1 cells (IL-10KO), increases the metastatic potential of melanoma cells. However, the molecule expressed on B-1 wt cells able to affect the metastatic potential of B16 cells remain to be fully explored. Therefore, the aim of this work was to identify the molecule expressed by B-1 wt, but absent in B-1 IL-10KO cells, which triggers increased metastatic potential of melanoma cells. Three independent experiments of microarrays analyses demonstrated differential mRNA expression of seven (7) genes between wt and IL-10KO B-1 cells. Among these genes, claudin-10, involved with cell communication and cell adhesion, was upregulated in B-1 wt cells. Data was confirmed by western blot analysis and interference RNA assays were performed to evaluate the biological function of claudin-10 in this model. Interestingly, silencing of claudin-10 expression on B-1 wt cells reduced their levels of ERK phosphorilation and prevent their capacity to increase the metastatic behavior of melanoma cells. Together, these findings suggest that claudin-10 expression on B-1 cells is crucial for their commitment to affect the metastatic potential of B16 melanoma cell. Acknowledgements Financial support: FAPESP References Almeida, S.R., L. S. Aroeira, et al.(2001).”Mouse B-1 cell-derived mononuclear phagocyte, a novel cellular component of acute non-specific inflammatory exudates”. Int Immunol 13(9):1193-201.. Fidler IJ (1973). "Selection of successive tumour lines for metastasis". Nat New Biol 242(118):148-9. Lopes, J. D. and M. Mariano (2009). "B-1 cell: the precursor of a novel mononuclear phagocyte with immuno-regulatory properties." An Acad Bras Cienc 81(3): 489-96.. Perez, E. C., J. Machado, Jr., et al. (2008). "B-1 lymphocytes increase metastatic behavior of melanoma cells through the extracellular signal-regulated kinase pathway." Cancer Sci 99(5): 920-8. Staquicini, F.I., C.R. Moreira, et al. (2003).”Enzyme and integrin expression by high and low metastatic melanoma cell lines”. Melanoma Res 13(1):11-8.. Staquicini, F. I., A. Tandle, et al. (2008). "A subset of host B lymphocytes controls melanoma metastasis through a melanoma cell adhesion molecule/MUC18-dependent interaction: evidence from mice and humans." Cancer Res 68(20): 8419-28.. Keywords: Melanoma, B-1 cells, claudin-10, metastases, Microarray Analysis Conference: 15th International Congress of Immunology (ICI), Milan, Italy, 22 Aug - 27 Aug, 2013. Presentation Type: Abstract Topic: Immune-mediated disease pathogenesis Citation: Perez EC, Xander P, Laurindo MF, EBrito RR, Vivanco B, Osugui L, Mariano M and Lopes JD (2013). Silencing of claudin-10 expression on B-1 cells impaired the increased metastatic behavior of melanoma cells an in vitro coculture system. Front. Immunol. Conference Abstract: 15th International Congress of Immunology (ICI). doi: 10.3389/conf.fimmu.2013.02.00975 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 26 Jun 2013; Published Online: 22 Aug 2013. * Correspondence: Prof. Elizabeth C Perez, Universisade Federal de São Paulo, São Paulo, Brazil, elicristin@hotmail.com Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Elizabeth C Perez Patricia Xander Maria F Laurindo Ronni R EBrito Bruno Vivanco Lika Osugui Mario Mariano José D Lopes Google Elizabeth C Perez Patricia Xander Maria F Laurindo Ronni R EBrito Bruno Vivanco Lika Osugui Mario Mariano José D Lopes Google Scholar Elizabeth C Perez Patricia Xander Maria F Laurindo Ronni R EBrito Bruno Vivanco Lika Osugui Mario Mariano José D Lopes PubMed Elizabeth C Perez Patricia Xander Maria F Laurindo Ronni R EBrito Bruno Vivanco Lika Osugui Mario Mariano José D Lopes Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.