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Loss of the EPH receptor B6 contributes to colorectal cancer metastasis.

Scientific reports (2017-03-07)
Silvia Mateo-Lozano, Sarah Bazzocco, Paulo Rodrigues, Rocco Mazzolini, Elena Andretta, Higinio Dopeso, Yolanda Fernández, Edgar Del Llano, Josipa Bilic, Lucía Suárez-López, Irati Macaya, Fernando Cartón-García, Rocio Nieto, Lizbeth M Jimenez-Flores, Priscila Guimarães de Marcondes, Yaiza Nuñez, Elsa Afonso, Karina Cacci, Javier Hernández-Losa, Stefania Landolfi, Ibane Abasolo, Santiago Ramón Y Cajal, John M Mariadason, Simo Schwartz, Toshimitsu Matsui, Diego Arango
RÉSUMÉ

Although 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

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Sigma-Aldrich
Anti-EPHB6 antibody produced in rabbit, affinity isolated antibody