<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>7(1)</volume><submitter>da Silva IL</submitter><pubmed_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 epithelial-mesenchymal 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 CD44&lt;sup>high&lt;/sup>/CD24&lt;sup>median/low&lt;/sup> cells. Remarkably, Qa-2 cell-surface expression was excluded from the CD44&lt;sup>high&lt;</pubmed_abstract><journal>Scientific reports</journal><pagination>6276</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC5524840</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Reduced expression of the murine HLA-G homolog Qa-2 is associated with malignancy, epithelial-mesenchymal transition and stemness in breast cancer cells.</pubmed_title><pmcid>PMC5524840</pmcid><pubmed_authors>Ferreira E</pubmed_authors><pubmed_authors>Toscano Simoes R</pubmed_authors><pubmed_authors>de Oliveira MC</pubmed_authors><pubmed_authors>Renart J</pubmed_authors><pubmed_authors>Soares Veloso E</pubmed_authors><pubmed_authors>Salviano Teixeira C</pubmed_authors><pubmed_authors>Martin-Villar E</pubmed_authors><pubmed_authors>Quintanilla M</pubmed_authors><pubmed_authors>Montero-Montero L</pubmed_authors><pubmed_authors>da Silva IL</pubmed_authors><pubmed_authors>Martin-Perez J</pubmed_authors><pubmed_authors>Sainz B</pubmed_authors></additional><is_claimable>false</is_claimable><name>Reduced expression of the murine HLA-G homolog Qa-2 is associated with malignancy, epithelial-mesenchymal transition and stemness in breast cancer cells.</name><description>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 epithelial-mesenchymal 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 CD44&lt;sup>high&lt;/sup>/CD24&lt;sup>median/low&lt;/sup> cells. Remarkably, Qa-2 cell-surface expression was excluded from the CD44&lt;sup>high&lt;</description><dates><release>2017-01-01T00:00:00Z</release><publication>2017 Jul</publication><modification>2025-06-01T01:39:25.04Z</modification><creation>2025-06-01T01:39:25.04Z</creation></dates><accession>S-EPMC5524840</accession><cross_references><pubmed>28740236</pubmed><doi>10.1038/s41598-017-06528-x</doi></cross_references></HashMap>