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Article: Reduced expression of EphB2 that parallels invasion and metastasis in colorectal tumours
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TitleReduced expression of EphB2 that parallels invasion and metastasis in colorectal tumours
 
AuthorsGuo, DL2
Zhang, J1 3
Yuen, ST2
Tsui, WY2
Chan, ASY2
Ho, C1
Ji, J3
Leung, SY2
Chen, X1
 
Issue Date2006
 
PublisherOxford University Press. The Journal's web site is located at http://carcin.oxfordjournals.org/
 
CitationCarcinogenesis, 2006, v. 27 n. 3, p. 454-464 [How to Cite?]
DOI: http://dx.doi.org/10.1093/carcin/bgi259
 
AbstractEphB2, a receptor tyrosine kinase regulated by the β-catenin/Tcf4 complex, is expressed in the proliferative compartment of mouse intestine and regulates bidirectional migration of intestinal precursor cells in the crypt-villus axis through repulsive interaction with Ephrin-B ligands. Recently, it has been shown that reduction of EphB activity accelerates colon tumour progression in the ApcMin/+ mice. In this study, we examined the expression of EphB2 in normal colon, adenomas, primary colorectal cancers (CRCs), lymph node metastases and liver metastases using immunohistochemistry on tissue microarrays. In addition, EphB2 was overexpressed in SW480 colon cancer cells to study its effect in vitro. We found that EphB2 was expressed in 100% of normal colon crypt base cells, 78% of adenomas, 55.4% of primary CRCs, 37.8% of lymph node metastases and 32.9% of liver metastases (all differences were statistically significant at P < 0.001 compared with primary CRCs). Patients with CRCs that lose EphB2 expression had more advanced tumour stage (P=0.005), poor differentiation (P=<0.001), poor overall survival (P=0.005) and disease-free survival (P=0.001), with the latter being independent of tumour stage. In vitro studies showed that overexpression of EphB2 inhibited colon cancer cell growth in colony formation assay and activation of EphB2 receptor inhibited colon cancer cell adhesion and migration. Our data demonstrated a progressive loss of EphB2 expression in each critical step of colon carcinogenesis, including the onset of invasion, dedifferentiation and metastasis which are paralleled by adverse patient outcome. EphB2 may achieve its tumour suppressor function through regulation of cell survival, adhesion and migration. © 2006 Oxford University Press.
 
ISSN0143-3334
2013 Impact Factor: 5.266
 
DOIhttp://dx.doi.org/10.1093/carcin/bgi259
 
ISI Accession Number IDWOS:000235771300011
 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorGuo, DL
 
dc.contributor.authorZhang, J
 
dc.contributor.authorYuen, ST
 
dc.contributor.authorTsui, WY
 
dc.contributor.authorChan, ASY
 
dc.contributor.authorHo, C
 
dc.contributor.authorJi, J
 
dc.contributor.authorLeung, SY
 
dc.contributor.authorChen, X
 
dc.date.accessioned2012-05-29T06:13:04Z
 
dc.date.available2012-05-29T06:13:04Z
 
dc.date.issued2006
 
dc.description.abstractEphB2, a receptor tyrosine kinase regulated by the β-catenin/Tcf4 complex, is expressed in the proliferative compartment of mouse intestine and regulates bidirectional migration of intestinal precursor cells in the crypt-villus axis through repulsive interaction with Ephrin-B ligands. Recently, it has been shown that reduction of EphB activity accelerates colon tumour progression in the ApcMin/+ mice. In this study, we examined the expression of EphB2 in normal colon, adenomas, primary colorectal cancers (CRCs), lymph node metastases and liver metastases using immunohistochemistry on tissue microarrays. In addition, EphB2 was overexpressed in SW480 colon cancer cells to study its effect in vitro. We found that EphB2 was expressed in 100% of normal colon crypt base cells, 78% of adenomas, 55.4% of primary CRCs, 37.8% of lymph node metastases and 32.9% of liver metastases (all differences were statistically significant at P < 0.001 compared with primary CRCs). Patients with CRCs that lose EphB2 expression had more advanced tumour stage (P=0.005), poor differentiation (P=<0.001), poor overall survival (P=0.005) and disease-free survival (P=0.001), with the latter being independent of tumour stage. In vitro studies showed that overexpression of EphB2 inhibited colon cancer cell growth in colony formation assay and activation of EphB2 receptor inhibited colon cancer cell adhesion and migration. Our data demonstrated a progressive loss of EphB2 expression in each critical step of colon carcinogenesis, including the onset of invasion, dedifferentiation and metastasis which are paralleled by adverse patient outcome. EphB2 may achieve its tumour suppressor function through regulation of cell survival, adhesion and migration. © 2006 Oxford University Press.
 
dc.description.naturelink_to_subscribed_fulltext
 
dc.identifier.citationCarcinogenesis, 2006, v. 27 n. 3, p. 454-464 [How to Cite?]
DOI: http://dx.doi.org/10.1093/carcin/bgi259
 
dc.identifier.citeulike526215
 
dc.identifier.doihttp://dx.doi.org/10.1093/carcin/bgi259
 
dc.identifier.epage464
 
dc.identifier.hkuros113971
 
dc.identifier.isiWOS:000235771300011
 
dc.identifier.issn0143-3334
2013 Impact Factor: 5.266
 
dc.identifier.issue3
 
dc.identifier.pmid16272170
 
dc.identifier.scopuseid_2-s2.0-33644866330
 
dc.identifier.spage454
 
dc.identifier.urihttp://hdl.handle.net/10722/148454
 
dc.identifier.volume27
 
dc.languageeng
 
dc.publisherOxford University Press. The Journal's web site is located at http://carcin.oxfordjournals.org/
 
dc.publisher.placeUnited Kingdom
 
dc.relation.ispartofCarcinogenesis
 
dc.relation.referencesReferences in Scopus
 
dc.rightsCarcinogenesis. Copyright © Oxford University Press.
 
dc.subject.meshAdenoma - Genetics - Pathology
 
dc.subject.meshAdult
 
dc.subject.meshAged
 
dc.subject.meshAged, 80 And Over
 
dc.subject.meshCell Survival
 
dc.subject.meshCell Transformation, Neoplastic
 
dc.subject.meshColon - Enzymology
 
dc.subject.meshColorectal Neoplasms - Genetics - Pathology
 
dc.subject.meshDisease-Free Survival
 
dc.subject.meshDown-Regulation
 
dc.subject.meshFemale
 
dc.subject.meshGene Expression Profiling
 
dc.subject.meshHumans
 
dc.subject.meshLiver Neoplasms - Secondary
 
dc.subject.meshLymphatic Metastasis
 
dc.subject.meshMale
 
dc.subject.meshMiddle Aged
 
dc.subject.meshNeoplasm Invasiveness
 
dc.subject.meshNeoplasm Metastasis
 
dc.subject.meshNeoplasm Staging
 
dc.subject.meshPrognosis
 
dc.subject.meshReceptor, Ephb2 - Biosynthesis
 
dc.titleReduced expression of EphB2 that parallels invasion and metastasis in colorectal tumours
 
dc.typeArticle
 
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<contributor.author>Chan, ASY</contributor.author>
<contributor.author>Ho, C</contributor.author>
<contributor.author>Ji, J</contributor.author>
<contributor.author>Leung, SY</contributor.author>
<contributor.author>Chen, X</contributor.author>
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Author Affiliations
  1. University of California, San Francisco
  2. The University of Hong Kong
  3. Peking University