Please use this identifier to cite or link to this item: http://ahro.austin.org.au/austinjspui/handle/1/19281
Title: Loss of the EPH receptor B6 contributes to colorectal cancer metastasis.
Authors: Mateo-Lozano, Silvia;Bazzocco, Sarah;Rodrigues, Paulo;Mazzolini, Rocco;Andretta, Elena;Dopeso, Higinio;Fernández, Yolanda;Del Llano, Edgar;Bilic, Josipa;Suárez-López, Lucía;Macaya, Irati;Cartón-García, Fernando;Nieto, Rocio;Jimenez-Flores, Lizbeth M;de Marcondes, Priscila Guimarães;Nuñez, Yaiza;Afonso, Elsa;Cacci, Karina;Hernández-Losa, Javier;Landolfi, Stefania;Abasolo, Ibane;Ramón Y Cajal, Santiago;Mariadason, John M;Schwartz, Simo;Matsui, Toshimitsu;Arango, Diego
Affiliation: Group of Drug Delivery and Targeting, CIBBIM-Nanomedicine, Vall d'Hebron University Hospital, Research Institute (VHIR), Universitat Autònoma de Barcelona, Barcelona, Spain
CIBER de Bioingeniería, Biomateriales y Nanomedicina (CIBER-BBN), Spain
Group of Drug Delivery and Targeting, CIBBIM-Nanomedicine, Vall d'Hebron University Hospital, Research Institute (VHIR), Universitat Autònoma de Barcelona, Barcelona, Spain.. Functional Validation &Preclinical Research (FVPR), Vall d'Hebron University Hospital, Research Institute (VHIR), Universitat Autònoma de Barcelona, Barcelona, Spain
Olivia Newton-John Cancer Research Institute, Heidelberg, Victoria, Australia
School of Cancer Medicine, La Trobe University, Melbourne, Australia
Group of Biomedical Research in Digestive Tract Tumors, CIBBIM-Nanomedicine, Vall d'Hebron University Hospital, Research Institute (VHIR), Universitat Autònoma de Barcelona, Barcelona, Spain
Department of Pathology, Vall d'Hebron Hospital, Barcelona, Spain (CIBERONC)
Hematology, Department of Medicine, Kobe University Graduate School of Medicine, Chuo-ku, Kobe, Japan
Issue Date: 6-Mar-2017
EDate: 2017-03-06
Citation: Scientific reports 2017; 7: 43702
Abstract: 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+/+ 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.
URI: http://ahro.austin.org.au/austinjspui/handle/1/19281
DOI: 10.1038/srep43702
PubMed URL: 28262839
Type: Journal Article
Research Support, Non-U.S. Gov't
Appears in Collections:Journal articles

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