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Article: The LIM domain protein, CRIP2, promotes apoptosis in esophageal squamous cell carcinoma

TitleThe LIM domain protein, CRIP2, promotes apoptosis in esophageal squamous cell carcinoma
Authors
KeywordsApoptosis
CRIP2
Esophageal squamous cell carcinoma
Issue Date2012
PublisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/canlet
Citation
Cancer Letters, 2012, v. 316 n. 1, p. 39-45 How to Cite?
AbstractThe group 2 LIM domain protein, Cysteine-rich intestinal protein 2 (CRIP2) was found to play an important role in esophageal squamous cell carcinoma (ESCC) tumorigenesis. Subcellular fractionation studies show that CRIP2 is expressed in the nucleus. Real-time quantitative PCR shows CRIP2 expression is down-regulated in ESCC tissues and cell lines. Functional studies reveal that CRIP2 reduces colony formation, growth, and invasion abilities. Furthermore, over-expression of CRIP2 induces apoptosis through induction of active caspases 3 and 9 proteins. In conclusion, this study shows CRIP2 plays an important role in the development of ESCC. © 2011 Elsevier Ireland Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/148676
ISSN
2015 Impact Factor: 5.992
2015 SCImago Journal Rankings: 2.331
ISI Accession Number ID
Funding AgencyGrant Number
Research Grants Council of the Hong Kong Special Administrative Region, People's Republic of ChinaHKU6615/07M
Funding Information:

The study was financed by the Research Grants Council of the Hong Kong Special Administrative Region, People's Republic of China: Grant number HKU6615/07M to MLL. We thank DSMZ (German Collection of Microorganisms and Cell Culture) for KYSE cell lines and acknowledge the use of the Faculty Core Facility of the Li Ka Shing Faculty of Medicine, HKU for flow cytometry.

References

 

DC FieldValueLanguage
dc.contributor.authorLo, PHYen_HK
dc.contributor.authorKo, JMYen_HK
dc.contributor.authorYu, ZYen_HK
dc.contributor.authorLaw, Sen_HK
dc.contributor.authorWang, LDen_HK
dc.contributor.authorLi, JLen_HK
dc.contributor.authorSrivastava, Gen_HK
dc.contributor.authorTsao, SWen_HK
dc.contributor.authorStanbridge, EJen_HK
dc.contributor.authorLung, MLen_HK
dc.date.accessioned2012-05-29T06:14:36Z-
dc.date.available2012-05-29T06:14:36Z-
dc.date.issued2012en_HK
dc.identifier.citationCancer Letters, 2012, v. 316 n. 1, p. 39-45en_HK
dc.identifier.issn0304-3835en_HK
dc.identifier.urihttp://hdl.handle.net/10722/148676-
dc.description.abstractThe group 2 LIM domain protein, Cysteine-rich intestinal protein 2 (CRIP2) was found to play an important role in esophageal squamous cell carcinoma (ESCC) tumorigenesis. Subcellular fractionation studies show that CRIP2 is expressed in the nucleus. Real-time quantitative PCR shows CRIP2 expression is down-regulated in ESCC tissues and cell lines. Functional studies reveal that CRIP2 reduces colony formation, growth, and invasion abilities. Furthermore, over-expression of CRIP2 induces apoptosis through induction of active caspases 3 and 9 proteins. In conclusion, this study shows CRIP2 plays an important role in the development of ESCC. © 2011 Elsevier Ireland Ltd.en_HK
dc.languageengen_US
dc.publisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/canleten_HK
dc.relation.ispartofCancer Lettersen_HK
dc.subjectApoptosisen_HK
dc.subjectCRIP2en_HK
dc.subjectEsophageal squamous cell carcinomaen_HK
dc.subject.meshAdaptor Proteins, Signal Transducing - genetics - metabolism-
dc.subject.meshApoptosis - genetics-
dc.subject.meshCarcinoma, Squamous Cell - genetics - metabolism - pathology-
dc.subject.meshEsophageal Neoplasms - genetics - metabolism - pathology-
dc.subject.meshLIM Domain Proteins - genetics - metabolism-
dc.titleThe LIM domain protein, CRIP2, promotes apoptosis in esophageal squamous cell carcinomaen_HK
dc.typeArticleen_HK
dc.identifier.emailLaw, S: slaw@hku.hken_HK
dc.identifier.emailSrivastava, G: gopesh@pathology.hku.hken_HK
dc.identifier.emailTsao, SW: gswtsao@hkucc.hku.hken_HK
dc.identifier.emailLung, ML: mlilung@hku.hken_HK
dc.identifier.authorityLaw, S=rp00437en_HK
dc.identifier.authoritySrivastava, G=rp00365en_HK
dc.identifier.authorityTsao, SW=rp00399en_HK
dc.identifier.authorityLung, ML=rp00300en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/j.canlet.2011.10.020en_HK
dc.identifier.pmid22154084-
dc.identifier.scopuseid_2-s2.0-84855342717en_HK
dc.identifier.hkuros199881-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-84855342717&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume316en_HK
dc.identifier.issue1en_HK
dc.identifier.spage39en_HK
dc.identifier.epage45en_HK
dc.identifier.isiWOS:000299712400006-
dc.publisher.placeIrelanden_HK
dc.identifier.scopusauthoridLo, PHY=36762664000en_HK
dc.identifier.scopusauthoridKo, JMY=35725559400en_HK
dc.identifier.scopusauthoridYu, ZY=54418314300en_HK
dc.identifier.scopusauthoridLaw, S=7202241293en_HK
dc.identifier.scopusauthoridWang, LD=35604729600en_HK
dc.identifier.scopusauthoridLi, JL=54417583000en_HK
dc.identifier.scopusauthoridSrivastava, G=7202242238en_HK
dc.identifier.scopusauthoridTsao, SW=7102813116en_HK
dc.identifier.scopusauthoridStanbridge, EJ=7103249410en_HK
dc.identifier.scopusauthoridLung, ML=7006411788en_HK
dc.identifier.citeulike9952982-

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