File Download
 
Links for fulltext
(May Require Subscription)
 
Supplementary

Article: Regulation of Nur77 expression by β-catenin and its mitogenic effect in colon cancer cells
  • Basic View
  • Metadata View
  • XML View
TitleRegulation of Nur77 expression by β-catenin and its mitogenic effect in colon cancer cells
 
AuthorsWu, H2
Lin, Y2
Li, W2
Sun, Z2
Gao, W2
Zhang, H2
Xie, L2
Jiang, F2
Qin, B2
Yan, T2
Chen, L2
Zhao, Y2
Cao, X1
Wu, Y1
Lin, B1
Zhou, H1
Wong, AST3
Zhang, XK2 1
Zeng, JZ2 2
 
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/
 
CitationFaseb Journal, 2011, v. 25 n. 1, p. 192-205 [How to Cite?]
DOI: http://dx.doi.org/10.1096/fj.10-166462
 
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.
 
ISSN0892-6638
2012 Impact Factor: 5.704
2012 SCImago Journal Rankings: 2.500
 
DOIhttp://dx.doi.org/10.1096/fj.10-166462
 
PubMed Central IDPMC3005431
 
ISI Accession Number IDWOS:000285869500018
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.

 
ReferencesReferences in Scopus
 
GrantsInvolvement of orphan nuclear receptor Nurr77 in regulating \xE1-catenin turnover and signaling
 
DC FieldValue
dc.contributor.authorWu, H
 
dc.contributor.authorLin, Y
 
dc.contributor.authorLi, W
 
dc.contributor.authorSun, Z
 
dc.contributor.authorGao, W
 
dc.contributor.authorZhang, H
 
dc.contributor.authorXie, L
 
dc.contributor.authorJiang, F
 
dc.contributor.authorQin, B
 
dc.contributor.authorYan, T
 
dc.contributor.authorChen, L
 
dc.contributor.authorZhao, Y
 
dc.contributor.authorCao, X
 
dc.contributor.authorWu, Y
 
dc.contributor.authorLin, B
 
dc.contributor.authorZhou, H
 
dc.contributor.authorWong, AST
 
dc.contributor.authorZhang, XK
 
dc.contributor.authorZeng, JZ
 
dc.date.accessioned2011-07-27T02:11:46Z
 
dc.date.available2011-07-27T02:11:46Z
 
dc.date.issued2011
 
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.
 
dc.description.naturelink_to_OA_fulltext
 
dc.identifier.citationFaseb Journal, 2011, v. 25 n. 1, p. 192-205 [How to Cite?]
DOI: http://dx.doi.org/10.1096/fj.10-166462
 
dc.identifier.doihttp://dx.doi.org/10.1096/fj.10-166462
 
dc.identifier.epage205
 
dc.identifier.hkuros188959
 
dc.identifier.isiWOS:000285869500018
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.

 
dc.identifier.issn0892-6638
2012 Impact Factor: 5.704
2012 SCImago Journal Rankings: 2.500
 
dc.identifier.issue1
 
dc.identifier.pmcidPMC3005431
 
dc.identifier.pmid20847229
 
dc.identifier.scopuseid_2-s2.0-78651376455
 
dc.identifier.spage192
 
dc.identifier.urihttp://hdl.handle.net/10722/136256
 
dc.identifier.volume25
 
dc.languageeng
 
dc.publisherFederation of American Societies for Experimental Biology. The Journal's web site is located at http://www.fasebj.org/
 
dc.publisher.placeUnited States
 
dc.relation.ispartofFASEB Journal
 
dc.relation.projectInvolvement of orphan nuclear receptor Nurr77 in regulating \xE1-catenin turnover and signaling
 
dc.relation.referencesReferences in Scopus
 
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.subjectAP-1
 
dc.subjectBile acid
 
dc.subjectJNK
 
dc.subjectPI3K
 
dc.titleRegulation of Nur77 expression by β-catenin and its mitogenic effect in colon cancer cells
 
dc.typeArticle
 
<?xml encoding="utf-8" version="1.0"?>
<item><contributor.author>Wu, H</contributor.author>
<contributor.author>Lin, Y</contributor.author>
<contributor.author>Li, W</contributor.author>
<contributor.author>Sun, Z</contributor.author>
<contributor.author>Gao, W</contributor.author>
<contributor.author>Zhang, H</contributor.author>
<contributor.author>Xie, L</contributor.author>
<contributor.author>Jiang, F</contributor.author>
<contributor.author>Qin, B</contributor.author>
<contributor.author>Yan, T</contributor.author>
<contributor.author>Chen, L</contributor.author>
<contributor.author>Zhao, Y</contributor.author>
<contributor.author>Cao, X</contributor.author>
<contributor.author>Wu, Y</contributor.author>
<contributor.author>Lin, B</contributor.author>
<contributor.author>Zhou, H</contributor.author>
<contributor.author>Wong, AST</contributor.author>
<contributor.author>Zhang, XK</contributor.author>
<contributor.author>Zeng, JZ</contributor.author>
<date.accessioned>2011-07-27T02:11:46Z</date.accessioned>
<date.available>2011-07-27T02:11:46Z</date.available>
<date.issued>2011</date.issued>
<identifier.citation>Faseb Journal, 2011, v. 25 n. 1, p. 192-205</identifier.citation>
<identifier.issn>0892-6638</identifier.issn>
<identifier.uri>http://hdl.handle.net/10722/136256</identifier.uri>
<description.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 &#946;-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/&#946;-catenin and AP-1 signaling pathways. &#169; FASEB.</description.abstract>
<language>eng</language>
<publisher>Federation of American Societies for Experimental Biology. The Journal&apos;s web site is located at http://www.fasebj.org/</publisher>
<relation.ispartof>FASEB Journal</relation.ispartof>
<subject>AP-1</subject>
<subject>Bile acid</subject>
<subject>JNK</subject>
<subject>PI3K</subject>
<subject.mesh>Cell Proliferation</subject.mesh>
<subject.mesh>Colonic Neoplasms - genetics - metabolism - pathology</subject.mesh>
<subject.mesh>Immunohistochemistry</subject.mesh>
<subject.mesh>Nuclear Receptor Subfamily 4, Group A, Member 1 - genetics - metabolism</subject.mesh>
<subject.mesh>beta Catenin - genetics - metabolism</subject.mesh>
<title>Regulation of Nur77 expression by &#946;-catenin and its mitogenic effect in colon cancer cells</title>
<type>Article</type>
<description.nature>link_to_OA_fulltext</description.nature>
<identifier.doi>10.1096/fj.10-166462</identifier.doi>
<identifier.pmid>20847229</identifier.pmid>
<identifier.pmcid>PMC3005431</identifier.pmcid>
<identifier.scopus>eid_2-s2.0-78651376455</identifier.scopus>
<identifier.hkuros>188959</identifier.hkuros>
<relation.references>http://www.scopus.com/mlt/select.url?eid=2-s2.0-78651376455&amp;selection=ref&amp;src=s&amp;origin=recordpage</relation.references>
<identifier.volume>25</identifier.volume>
<identifier.issue>1</identifier.issue>
<identifier.spage>192</identifier.spage>
<identifier.epage>205</identifier.epage>
<identifier.isi>WOS:000285869500018</identifier.isi>
<publisher.place>United States</publisher.place>
<relation.project>Involvement of orphan nuclear receptor Nurr77 in regulating \xE1-catenin turnover and signaling</relation.project>
<bitstream.url>http://hub.hku.hk/bitstream/10722/136256/1/re01.htm</bitstream.url>
</item>
Author Affiliations
  1. Sanford-Burnham Medical Research Institute
  2. Xiamen University
  3. The University of Hong Kong