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Article: Regulation of Nur77 expression by β-catenin and its mitogenic effect in colon cancer cells

TitleRegulation of Nur77 expression by β-catenin and its mitogenic effect in colon cancer cells
Authors
KeywordsAP-1
Bile acid
JNK
PI3K
Issue Date2011
PublisherFederation of American Societies for Experimental Biology. The Journal's web site is located at http://www.fasebj.org/
Citation
Faseb Journal, 2011, v. 25 n. 1, p. 192-205 How to Cite?
Abstract
The orphan nuclear receptor Nur77 is an immediate-early response gene whose expression is rapidly induced by various extracellular stimuli. The aims of this study were to study the role of Nur77 expression in the growth and survival of colon cancer cells and the mechanism by which Nur77 expression was regulated. We showed that levels of Nur77 were elevated in a majority of human colon tumors (9/12) compared to their nontumorous tissues and that Nur77 expression could be strongly induced by different colonic carcinogens including deoxycholic acid (DCA). DCA-induced Nur77 expression resulted in up-regulation of antiapoptotic BRE and angiogenic VEGF, and it enhanced the growth, colony formation, and migration of colon cancer cells. In studying the mechanism by which Nur77 was regulated in colon cancer cells, we found that β-catenin was involved in induction of Nur77 expression through its activation of the transcriptional activity of AP-1 (c-Fos/c-Jun) that bound to and transactivated the Nur77 promoter. Together, our results demonstrate that Nur77 acts to promote the growth and survival of colon cancer cells and serves as an important mediator of the Wnt/β-catenin and AP-1 signaling pathways. © FASEB.
Persistent Identifierhttp://hdl.handle.net/10722/136256
ISSN
2013 Impact Factor: 5.480
PubMed Central ID
ISI Accession Number ID
Funding AgencyGrant Number
863 Program2007AA09Z404
National Natural Science Foundation of China (NSFC)30971445
Key Science and Technology Planning Project2007I0023
Natural Science Foundation of Fujian Province, China2009J01198
NSFC/Hong Kong Research Grants Council (RGC)30931160431
U.S. National Institutes of HealthCA109345
CA140980
GM089927
U.S. Army Medical Research and Material CommandPCRPW81XWH-08-1-0478
Natural Science Foundation of Fujian Province2008Y0062
N_HKU 735/09
Funding Information:

This work was in part supported by grants to J.-Z.Z. from the 863 Program (2007AA09Z404), the National Natural Science Foundation of China (NSFC; 30971445), the Key Science and Technology Planning Project (2007I0023), the Natural Science Foundation of Fujian Province, China (2009J01198), and the NSFC/Hong Kong Research Grants Council (RGC; 30931160431), a grant to A.S.-T.W. (N_HKU 735/09), and grants to X.Z. from the U.S. National Institutes of Health (CA109345, CA140980, GM089927), the U.S. Army Medical Research and Material Command (PCRPW81XWH-08-1-0478), and the Natural Science Foundation of Fujian Province (2008Y0062). The authors declare no conflicts of interest.

References
Grants

 

Author Affiliations
  1. Sanford-Burnham Medical Research Institute
  2. Xiamen University
  3. The University of Hong Kong
DC FieldValueLanguage
dc.contributor.authorWu, Hen_HK
dc.contributor.authorLin, Yen_HK
dc.contributor.authorLi, Wen_HK
dc.contributor.authorSun, Zen_HK
dc.contributor.authorGao, Wen_HK
dc.contributor.authorZhang, Hen_HK
dc.contributor.authorXie, Len_HK
dc.contributor.authorJiang, Fen_HK
dc.contributor.authorQin, Ben_HK
dc.contributor.authorYan, Ten_HK
dc.contributor.authorChen, Len_HK
dc.contributor.authorZhao, Yen_HK
dc.contributor.authorCao, Xen_HK
dc.contributor.authorWu, Yen_HK
dc.contributor.authorLin, Ben_HK
dc.contributor.authorZhou, Hen_HK
dc.contributor.authorWong, ASTen_HK
dc.contributor.authorZhang, XKen_HK
dc.contributor.authorZeng, JZen_HK
dc.date.accessioned2011-07-27T02:11:46Z-
dc.date.available2011-07-27T02:11:46Z-
dc.date.issued2011en_HK
dc.identifier.citationFaseb Journal, 2011, v. 25 n. 1, p. 192-205en_HK
dc.identifier.issn0892-6638en_HK
dc.identifier.urihttp://hdl.handle.net/10722/136256-
dc.description.abstractThe orphan nuclear receptor Nur77 is an immediate-early response gene whose expression is rapidly induced by various extracellular stimuli. The aims of this study were to study the role of Nur77 expression in the growth and survival of colon cancer cells and the mechanism by which Nur77 expression was regulated. We showed that levels of Nur77 were elevated in a majority of human colon tumors (9/12) compared to their nontumorous tissues and that Nur77 expression could be strongly induced by different colonic carcinogens including deoxycholic acid (DCA). DCA-induced Nur77 expression resulted in up-regulation of antiapoptotic BRE and angiogenic VEGF, and it enhanced the growth, colony formation, and migration of colon cancer cells. In studying the mechanism by which Nur77 was regulated in colon cancer cells, we found that β-catenin was involved in induction of Nur77 expression through its activation of the transcriptional activity of AP-1 (c-Fos/c-Jun) that bound to and transactivated the Nur77 promoter. Together, our results demonstrate that Nur77 acts to promote the growth and survival of colon cancer cells and serves as an important mediator of the Wnt/β-catenin and AP-1 signaling pathways. © FASEB.en_HK
dc.languageengen_US
dc.publisherFederation of American Societies for Experimental Biology. The Journal's web site is located at http://www.fasebj.org/en_HK
dc.relation.ispartofFASEB Journalen_HK
dc.subjectAP-1en_HK
dc.subjectBile aciden_HK
dc.subjectJNKen_HK
dc.subjectPI3Ken_HK
dc.subject.meshCell Proliferation-
dc.subject.meshColonic Neoplasms - genetics - metabolism - pathology-
dc.subject.meshImmunohistochemistry-
dc.subject.meshNuclear Receptor Subfamily 4, Group A, Member 1 - genetics - metabolism-
dc.subject.meshbeta Catenin - genetics - metabolism-
dc.titleRegulation of Nur77 expression by β-catenin and its mitogenic effect in colon cancer cellsen_HK
dc.typeArticleen_HK
dc.identifier.emailWong, AST: awong1@hkucc.hku.hken_HK
dc.identifier.authorityWong, AST=rp00805en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1096/fj.10-166462en_HK
dc.identifier.pmid20847229en_HK
dc.identifier.pmcidPMC3005431-
dc.identifier.scopuseid_2-s2.0-78651376455en_HK
dc.identifier.hkuros188959en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-78651376455&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume25en_HK
dc.identifier.issue1en_HK
dc.identifier.spage192en_HK
dc.identifier.epage205en_HK
dc.identifier.isiWOS:000285869500018-
dc.publisher.placeUnited Statesen_HK
dc.relation.projectInvolvement of orphan nuclear receptor Nurr77 in regulating \xE1-catenin turnover and signaling-
dc.identifier.scopusauthoridWu, H=7405579131en_HK
dc.identifier.scopusauthoridLin, Y=37361145300en_HK
dc.identifier.scopusauthoridLi, W=37361306100en_HK
dc.identifier.scopusauthoridSun, Z=37361638600en_HK
dc.identifier.scopusauthoridGao, W=36460914100en_HK
dc.identifier.scopusauthoridZhang, H=37361771100en_HK
dc.identifier.scopusauthoridXie, L=36464671300en_HK
dc.identifier.scopusauthoridJiang, F=55419707100en_HK
dc.identifier.scopusauthoridQin, B=37361344700en_HK
dc.identifier.scopusauthoridYan, T=25634571800en_HK
dc.identifier.scopusauthoridChen, L=37361045900en_HK
dc.identifier.scopusauthoridZhao, Y=36464669500en_HK
dc.identifier.scopusauthoridCao, X=7403370589en_HK
dc.identifier.scopusauthoridWu, Y=36462161800en_HK
dc.identifier.scopusauthoridLin, B=7403507995en_HK
dc.identifier.scopusauthoridZhou, H=35249970700en_HK
dc.identifier.scopusauthoridWong, AST=23987963300en_HK
dc.identifier.scopusauthoridZhang, XK=35742430100en_HK
dc.identifier.scopusauthoridZeng, JZ=7402652375en_HK

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