dc.contributor.author | L. da Silva, Istéfani | |
dc.contributor.author | Montero Montero, Lucía | |
dc.contributor.author | Martín Villar, Ester | |
dc.contributor.author | Martín Pérez, Jorge | |
dc.contributor.author | Sainz, Bruno | |
dc.contributor.author | Renart, Jaime | |
dc.contributor.author | Toscano Simões, Renata | |
dc.contributor.author | Soares Veloso, Émerson | |
dc.contributor.author | Salviano Teixeira, Cláudia | |
dc.contributor.author | C. de Oliveira, Mônica | |
dc.contributor.author | Ferreira, Enio | |
dc.contributor.author | Quintanilla, Miguel | |
dc.date.accessioned | 2020-01-15T13:01:21Z | |
dc.date.available | 2020-01-15T13:01:21Z | |
dc.date.issued | 2017 | |
dc.identifier.issn | 2045-2322 | spa |
dc.identifier.uri | http://hdl.handle.net/10641/1792 | |
dc.description.abstract | Qa-2 is believed to mediate a protective immune response against cancer; however, little is known
about the role of Qa-2 in tumorigenesis. Here, we used 4T1 breast cancer cells to study the involvement
of Qa-2 in tumor progression in a syngeneic host. Qa-2 expression was reduced during in vivo tumor
growth and in cell lines derived from 4T1-induced tumors. Tumor-derived cells elicited an epithelialmesenchymal
transition associated with upregulation of Zeb1 and Twist1/2 and enhanced tumor
initiating and invasive capacities. Furthermore, these cells showed increased stem characteristics, as
demonstrated by upregulation of Hes1, Sox2 and Oct3/4, and enrichment of CD44high/CD24median/low
cells. Remarkably, Qa-2 cell-surface expression was excluded from the CD44high/CD24median/low
subpopulation. Tumor-derived cells showed increased Src activity, and treatment of these cells with the
Src kinase inhibitor PP2 enhanced Qa-2 but reduced Sox2 and CD44high/CD24median/low expression levels,
suggesting that Src signaling, while positively associated with stemness, negatively regulates Qa-2
expression in breast cancer. Finally, overexpression of the Qa-2 family member Q7 on the cell surface
slowed down in vivo tumor growth and reduced the metastatic potential of 4T1 cells. These results
suggest an anti-malignant role for Qa-2 in breast cancer development, which appears to be absent from
cancer stem cells. | spa |
dc.language.iso | eng | spa |
dc.publisher | Scientific Reports | spa |
dc.rights | Atribución-NoComercial-SinDerivadas 3.0 España | * |
dc.rights.uri | http://creativecommons.org/licenses/by-nc-nd/3.0/es/ | * |
dc.title | Reduced expression of the murine HLA-G homolog Qa-2 is associated with malignancy, epithelialmesenchymal transition and stemness in breast cancer cells. | spa |
dc.type | journal article | spa |
dc.type.hasVersion | AM | spa |
dc.rights.accessRights | open access | spa |
dc.description.extent | 2122 KB | spa |
dc.identifier.doi | 10.1038/s41598-017-06528-x | spa |
dc.relation.publisherversion | https://www.nature.com/articles/s41598-017-06528-x | spa |