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dc.contributor.authorMateo-Lozano, Silvia
dc.contributor.authorBazzocco, Sarah
dc.contributor.authorRodrigues, Paulo
dc.contributor.authorMazzolini, Rocco
dc.contributor.authorAndretta, Elena
dc.contributor.authorDopeso, Higinio
dc.contributor.authorFernández, Yolanda
dc.contributor.authorDel Llano, Edgar
dc.contributor.authorBilic, Josipa
dc.contributor.authorSuárez-López, Lucía
dc.contributor.authorMacaya, Irati
dc.contributor.authorCartón-García, Fernando
dc.contributor.authorNieto, Rocio
dc.contributor.authorJimenez-Flores, Lizbeth M
dc.contributor.authorde Marcondes, Priscila Guimarães
dc.contributor.authorNuñez, Yaiza
dc.contributor.authorAfonso, Elsa
dc.contributor.authorCacci, Karina
dc.contributor.authorHernández-Losa, Javier
dc.contributor.authorLandolfi, Stefania
dc.contributor.authorAbasolo, Ibane
dc.contributor.authorRamón Y Cajal, Santiago
dc.contributor.authorMariadason, John M
dc.contributor.authorSchwartz, Simo
dc.contributor.authorMatsui, Toshimitsu
dc.contributor.authorArango, Diego
dc.identifier.citationSci Rep.2017 03;(7):43702
dc.description.abstractAlthough deregulation of EPHB signaling has been shown to be an important step in colorectal tumorigenesis, the role of EPHB6 in this process has not been investigated. We found here that manipulation of EPHB6 levels in colon cancer cell lines has no effect on their motility and growth on a solid substrate, soft agar or in a xenograft mouse model. We then used an EphB6 knockout mouse model to show that EphB6 inactivation does not efficiently initiate tumorigenesis in the intestinal tract. In addition, when intestinal tumors are initiated genetically or pharmacologically in EphB6+/+ and EphB6-/- mice, no differences were observed in animal survival, tumor multiplicity, size or histology, and proliferation of intestinal epithelial cells or tumor cells. However, reintroduction of EPHB6 into colon cancer cells significantly reduced the number of lung metastasis after tail-vein injection in immunodeficient mice, while EPHB6 knockdown in EPHB6-expressing cells increased their metastatic spread. Consistently, although EPHB6 protein expression in a series of 130 primary colorectal tumors was not associated with patient survival, EPHB6 expression was significantly lower in lymph node metastases compared to primary tumors. Our results indicate that the loss of EPHB6 contributes to the metastatic process of colorectal cancer.
dc.subject.meshCell Line, Tumor
dc.subject.meshCell Movement
dc.subject.meshCell Proliferation
dc.subject.meshCell Transformation, Neoplastic
dc.subject.meshColorectal Neoplasms
dc.subject.meshDisease Models, Animal
dc.subject.meshGene Expression
dc.subject.meshMice, Knockout
dc.subject.meshNeoplasm Metastasis
dc.subject.meshNeoplasm Staging
dc.subject.meshReceptors, Eph Family
dc.subject.meshBiomarkers, Tumor
dc.titleLoss of the EPH receptor B6 contributes to colorectal cancer metastasis.
dc.identifier.journalScientific reports
dc.pubmedtypeJournal Article
dc.pubmedtypeResearch Support, Non-U.S. Gov't
Appears in Collections:Fundaciones e Institutos de Investigación > IIS H. U. Ramón y Cajal > Artículos

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