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Article: Cysteine-rich intestinal protein 2 (CRIP2) acts as a repressor of NF-κB-mediated proangiogenic cytokine transcription to suppress tumorigenesis and angiogenesis
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TitleCysteine-rich intestinal protein 2 (CRIP2) acts as a repressor of NF-κB-mediated proangiogenic cytokine transcription to suppress tumorigenesis and angiogenesis
 
AuthorsCheung, AKL3
Ko, JMY3
Lung, HL3
Chan, KW3
Stanbridge, EJ4
Zabarovsky, E1 5
Tokino, T2
Kashima, L2
Suzuki, T6
Kwong, DLW3
Chua, D3
Tsao, SW3
Lung, ML3
 
KeywordsAntiangiogenesis
Transcription regulator
 
Issue Date2011
 
PublisherNational Academy of Sciences. The Journal's web site is located at http://www.pnas.org
 
CitationProceedings Of The National Academy Of Sciences Of The United States Of America, 2011, v. 108 n. 20, p. 8390-8395 [How to Cite?]
DOI: http://dx.doi.org/10.1073/pnas.1101747108
 
AbstractChromosome 14 was transferred into tumorigenic nasopharyngeal carcinoma and esophageal carcinoma cell lines by a microcell-mediated chromosome transfer approach. Functional complementation of defects present in the cancer cells suppressed tumor formation. A candidate tumor-suppressor gene, cysteine-rich intestinal protein 2 (CRIP2), located in the hot spot for chromosomal loss at 14q32.3, was identified as an important candidate gene capable of functionally suppressing tumor formation. Previous studies have shown that CRIP2 is associated with development. To date, no report has provided functional evidence supporting a role for CRIP2 in tumor development. The present study provides unequivocal evidence that CRIP2 can functionally suppress tumorigenesis. CRIP2 is significantly down-regulated in nasopharyngeal carcinoma cell lines and tumors. CRIP2 reexpression functionally suppresses in vivo tumorigenesis and angiogenesis; these effects are induced by its transcription-repressor capability. It interacts with the NF-κB/p65 to inhibit its DNA-binding ability to the promoter regions of the major proangiogenesis cytokines critical for tumor progression, including IL6, IL8, and VEGF. In conclusion, we provide compelling evidence that CRIP2 acts as a transcription repressor of the NF-κB-mediated proangiogenic cytokine expression and thus functionally inhibits tumor formation and angiogenesis.
 
ISSN0027-8424
2012 Impact Factor: 9.737
2012 SCImago Journal Rankings: 5.473
 
DOIhttp://dx.doi.org/10.1073/pnas.1101747108
 
PubMed Central IDPMC3100921
 
ISI Accession Number IDWOS:000290719600063
Funding AgencyGrant Number
Research Grants Council
University Grants Council of the Hong Kong Special Administrative Region, People's Republic of China6615/07M
AoE/M-06/08
University of Hong Kong200907176081
Swedish Cancer Society
Swedish Research Council
Swedish Institute
Royal Swedish Academy of Sciences
Karolinska Institute
Funding Information:

This work was supported by the Research Grants Council and the University Grants Council of the Hong Kong Special Administrative Region, People's Republic of China (Grants 6615/07M and AoE/M-06/08, to M. L. L.); the University of Hong Kong Small Project Fund (Grant 200907176081, to A. K. L. C.); and the Swedish Cancer Society, Swedish Research Council, Swedish Institute, Royal Swedish Academy of Sciences, and Karolinska Institute (E.Z.).

 
ReferencesReferences in Scopus
 
GrantsCentre for Nasopharyngeal Carcinoma Research
 
DC FieldValue
dc.contributor.authorCheung, AKL
 
dc.contributor.authorKo, JMY
 
dc.contributor.authorLung, HL
 
dc.contributor.authorChan, KW
 
dc.contributor.authorStanbridge, EJ
 
dc.contributor.authorZabarovsky, E
 
dc.contributor.authorTokino, T
 
dc.contributor.authorKashima, L
 
dc.contributor.authorSuzuki, T
 
dc.contributor.authorKwong, DLW
 
dc.contributor.authorChua, D
 
dc.contributor.authorTsao, SW
 
dc.contributor.authorLung, ML
 
dc.date.accessioned2011-08-26T14:18:34Z
 
dc.date.available2011-08-26T14:18:34Z
 
dc.date.issued2011
 
dc.description.abstractChromosome 14 was transferred into tumorigenic nasopharyngeal carcinoma and esophageal carcinoma cell lines by a microcell-mediated chromosome transfer approach. Functional complementation of defects present in the cancer cells suppressed tumor formation. A candidate tumor-suppressor gene, cysteine-rich intestinal protein 2 (CRIP2), located in the hot spot for chromosomal loss at 14q32.3, was identified as an important candidate gene capable of functionally suppressing tumor formation. Previous studies have shown that CRIP2 is associated with development. To date, no report has provided functional evidence supporting a role for CRIP2 in tumor development. The present study provides unequivocal evidence that CRIP2 can functionally suppress tumorigenesis. CRIP2 is significantly down-regulated in nasopharyngeal carcinoma cell lines and tumors. CRIP2 reexpression functionally suppresses in vivo tumorigenesis and angiogenesis; these effects are induced by its transcription-repressor capability. It interacts with the NF-κB/p65 to inhibit its DNA-binding ability to the promoter regions of the major proangiogenesis cytokines critical for tumor progression, including IL6, IL8, and VEGF. In conclusion, we provide compelling evidence that CRIP2 acts as a transcription repressor of the NF-κB-mediated proangiogenic cytokine expression and thus functionally inhibits tumor formation and angiogenesis.
 
dc.description.naturelink_to_OA_fulltext
 
dc.identifier.citationProceedings Of The National Academy Of Sciences Of The United States Of America, 2011, v. 108 n. 20, p. 8390-8395 [How to Cite?]
DOI: http://dx.doi.org/10.1073/pnas.1101747108
 
dc.identifier.doihttp://dx.doi.org/10.1073/pnas.1101747108
 
dc.identifier.eissn1091-6490
 
dc.identifier.epage8395
 
dc.identifier.hkuros190806
 
dc.identifier.isiWOS:000290719600063
Funding AgencyGrant Number
Research Grants Council
University Grants Council of the Hong Kong Special Administrative Region, People's Republic of China6615/07M
AoE/M-06/08
University of Hong Kong200907176081
Swedish Cancer Society
Swedish Research Council
Swedish Institute
Royal Swedish Academy of Sciences
Karolinska Institute
Funding Information:

This work was supported by the Research Grants Council and the University Grants Council of the Hong Kong Special Administrative Region, People's Republic of China (Grants 6615/07M and AoE/M-06/08, to M. L. L.); the University of Hong Kong Small Project Fund (Grant 200907176081, to A. K. L. C.); and the Swedish Cancer Society, Swedish Research Council, Swedish Institute, Royal Swedish Academy of Sciences, and Karolinska Institute (E.Z.).

 
dc.identifier.issn0027-8424
2012 Impact Factor: 9.737
2012 SCImago Journal Rankings: 5.473
 
dc.identifier.issue20
 
dc.identifier.pmcidPMC3100921
 
dc.identifier.pmid21540330
 
dc.identifier.scopuseid_2-s2.0-79957787635
 
dc.identifier.spage8390
 
dc.identifier.urihttp://hdl.handle.net/10722/137193
 
dc.identifier.volume108
 
dc.languageeng
 
dc.publisherNational Academy of Sciences. The Journal's web site is located at http://www.pnas.org
 
dc.publisher.placeUnited States
 
dc.relation.ispartofProceedings of the National Academy of Sciences of the United States of America
 
dc.relation.projectCentre for Nasopharyngeal Carcinoma Research
 
dc.relation.referencesReferences in Scopus
 
dc.subject.meshAdaptor Proteins, Signal Transducing - physiology
 
dc.subject.meshCell Transformation, Neoplastic - genetics
 
dc.subject.meshCytokines - genetics - physiology
 
dc.subject.meshNF-kappa B - metabolism
 
dc.subject.meshNeovascularization, Pathologic - genetics
 
dc.subjectAntiangiogenesis
 
dc.subjectTranscription regulator
 
dc.titleCysteine-rich intestinal protein 2 (CRIP2) acts as a repressor of NF-κB-mediated proangiogenic cytokine transcription to suppress tumorigenesis and angiogenesis
 
dc.typeArticle
 
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Author Affiliations
  1. Karolinska University Hospital
  2. Sapporo Medical University
  3. The University of Hong Kong
  4. UC Irvine
  5. Engelhardt Institute of Molecular Biology, Russian Academy of Sciences
  6. Hokkaido University