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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

TitleCysteine-rich intestinal protein 2 (CRIP2) acts as a repressor of NF-κB-mediated proangiogenic cytokine transcription to suppress tumorigenesis and angiogenesis
Authors
KeywordsAntiangiogenesis
Transcription regulator
Issue Date2011
PublisherNational Academy of Sciences. The Journal's web site is located at http://www.pnas.org
Citation
Proceedings Of The National Academy Of Sciences Of The United States Of America, 2011, v. 108 n. 20, p. 8390-8395 How to Cite?
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.
Persistent Identifierhttp://hdl.handle.net/10722/137193
ISSN
2014 Impact Factor: 9.674
2014 SCImago Journal Rankings: 5.781
PubMed Central ID
ISI Accession Number ID
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.).

References
Grants

 

DC FieldValueLanguage
dc.contributor.authorCheung, AKLen_HK
dc.contributor.authorKo, JMYen_HK
dc.contributor.authorLung, HLen_HK
dc.contributor.authorChan, KWen_HK
dc.contributor.authorStanbridge, EJen_HK
dc.contributor.authorZabarovsky, Een_HK
dc.contributor.authorTokino, Ten_HK
dc.contributor.authorKashima, Len_HK
dc.contributor.authorSuzuki, Ten_HK
dc.contributor.authorKwong, DLWen_HK
dc.contributor.authorChua, Den_HK
dc.contributor.authorTsao, SWen_HK
dc.contributor.authorLung, MLen_HK
dc.date.accessioned2011-08-26T14:18:34Z-
dc.date.available2011-08-26T14:18:34Z-
dc.date.issued2011en_HK
dc.identifier.citationProceedings Of The National Academy Of Sciences Of The United States Of America, 2011, v. 108 n. 20, p. 8390-8395en_HK
dc.identifier.issn0027-8424en_HK
dc.identifier.urihttp://hdl.handle.net/10722/137193-
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.en_HK
dc.languageengen_US
dc.publisherNational Academy of Sciences. The Journal's web site is located at http://www.pnas.orgen_HK
dc.relation.ispartofProceedings of the National Academy of Sciences of the United States of Americaen_HK
dc.subjectAntiangiogenesisen_HK
dc.subjectTranscription regulatoren_HK
dc.subject.meshAdaptor Proteins, Signal Transducing - physiologyen_HK
dc.subject.meshCell Transformation, Neoplastic - geneticsen_HK
dc.subject.meshCytokines - genetics - physiologyen_HK
dc.subject.meshNF-kappa B - metabolismen_HK
dc.subject.meshNeovascularization, Pathologic - geneticsen_HK
dc.titleCysteine-rich intestinal protein 2 (CRIP2) acts as a repressor of NF-κB-mediated proangiogenic cytokine transcription to suppress tumorigenesis and angiogenesisen_HK
dc.typeArticleen_HK
dc.identifier.emailCheung, AKL: arthurhk@hku.hken_HK
dc.identifier.emailLung, HL: hllung2@hku.hken_HK
dc.identifier.emailChan, KW: hrmtckw@hkucc.hku.hken_HK
dc.identifier.emailKwong, DLW: dlwkwong@hku.hken_HK
dc.identifier.emailChua, D: dttchua@hkucc.hku.hken_HK
dc.identifier.emailTsao, SW: gswtsao@hkucc.hku.hken_HK
dc.identifier.emailLung, ML: mlilung@hku.hken_HK
dc.identifier.authorityCheung, AKL=rp01769en_HK
dc.identifier.authorityLung, HL=rp00299en_HK
dc.identifier.authorityChan, KW=rp00330en_HK
dc.identifier.authorityKwong, DLW=rp00414en_HK
dc.identifier.authorityChua, D=rp00415en_HK
dc.identifier.authorityTsao, SW=rp00399en_HK
dc.identifier.authorityLung, ML=rp00300en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1073/pnas.1101747108en_HK
dc.identifier.pmid21540330en_HK
dc.identifier.pmcidPMC3100921-
dc.identifier.scopuseid_2-s2.0-79957787635en_HK
dc.identifier.hkuros190806en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-79957787635&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume108en_HK
dc.identifier.issue20en_HK
dc.identifier.spage8390en_HK
dc.identifier.epage8395en_HK
dc.identifier.eissn1091-6490-
dc.identifier.isiWOS:000290719600063-
dc.publisher.placeUnited Statesen_HK
dc.relation.projectCentre for Nasopharyngeal Carcinoma Research-
dc.identifier.scopusauthoridCheung, AKL=8967932600en_HK
dc.identifier.scopusauthoridKo, JMY=35725559400en_HK
dc.identifier.scopusauthoridLung, HL=6603819904en_HK
dc.identifier.scopusauthoridChan, KW=16444133100en_HK
dc.identifier.scopusauthoridStanbridge, EJ=7103249410en_HK
dc.identifier.scopusauthoridZabarovsky, E=7007009108en_HK
dc.identifier.scopusauthoridTokino, T=7005103751en_HK
dc.identifier.scopusauthoridKashima, L=8849149200en_HK
dc.identifier.scopusauthoridSuzuki, T=7409095163en_HK
dc.identifier.scopusauthoridKwong, DLW=15744231600en_HK
dc.identifier.scopusauthoridChua, D=7006773480en_HK
dc.identifier.scopusauthoridTsao, SW=7102813116en_HK
dc.identifier.scopusauthoridLung, ML=7006411788en_HK

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