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Article: Cell cycle-related kinase supports ovarian carcinoma cell proliferation via regulation of cyclin D1 and is a predictor of outcome in patients with ovarian carcinoma

TitleCell cycle-related kinase supports ovarian carcinoma cell proliferation via regulation of cyclin D1 and is a predictor of outcome in patients with ovarian carcinoma
Authors
KeywordsCell cycle
Cell cycle-related kinase
Cyclin D1
Ovarian cancer
Prognosis
Issue Date2009
PublisherJohn Wiley & Sons, Inc.. The Journal's web site is located at http://www3.interscience.wiley.com/journal/29331/home
Citation
International Journal Of Cancer, 2009, v. 125 n. 11, p. 2631-2642 How to Cite?
AbstractOur previous study has suggested that the cell cycle-related kinase (CCRK) is a putative candidate oncogene in glioblastoma tumorigenesis. The potential oncogenic role of CCRK and its clinical/prognostic significance, however, in ovarian carcinoma are unclear. In this study, CCRK expression was examined by immunohistochemistry in a series of ovarian carcinoma tissues. Overexpression of CCRK was detected in 53% of the ovarian carcinomas, and it was positively correlated with an ascending histological grade and/or advanced clinical stage of the disease (p < 0.05). In addition, overexpression of CCRK in ovarian carcinoma was determined to be a strong and an independent predictor of short overall survival (p < 0.05). In ovarian carcinoma cells, CCRK knockdown by RNAi led to a G1 phase cell cycle arrest, while CCRK overexpression by stable transfection of CCRK-containing plasmid pcDNA-CCRK promoted cell proliferation in vitro and tumor growth in vivo. In addition, CCRK knockdown was found to reduce cyclin D1 expression. Consistently, CCRK overexpression increased cyclin D1 expression, and furthermore, a significant correlation between expression of CCRK and cyclin D1 in ovarian carcinomas was observed (p < 0.001). These findings suggest a potential important role of CCRK in the control of cell proliferation via regulation of cyclin D1 expression, and the overexpression of CCRK, as detected by immunohistochemistry, is an independent molecular marker for shortened survival time of patients with ovarian carcinoma. © 2009 UICC.
Persistent Identifierhttp://hdl.handle.net/10722/68107
ISSN
2015 Impact Factor: 5.531
2015 SCImago Journal Rankings: 2.657
ISI Accession Number ID
Funding AgencyGrant Number
Major State Basic Research Program of China2006CB910104
Nature Science Foundation of China30772334
Key Special Project of Guangdong Science and Technology Agency2005A30801001
Funding Information:

Grant sponsor Major State Basic Research Program of China: Grant number 2006CB910104. Grant sponsor: Nature Science Foundation of China: Grant number: 30772334. Grain sponsor: Key Special Project of Guangdong Science and Technology Agency; Grant number 2005A30801001.

References

 

DC FieldValueLanguage
dc.contributor.authorWu, GQen_HK
dc.contributor.authorXie, Den_HK
dc.contributor.authorYang, GFen_HK
dc.contributor.authorLiao, YJen_HK
dc.contributor.authorMai, SJen_HK
dc.contributor.authorDeng, HXen_HK
dc.contributor.authorSze, Jen_HK
dc.contributor.authorGuan, XYen_HK
dc.contributor.authorZeng, YXen_HK
dc.contributor.authorLin, MCen_HK
dc.contributor.authorKung, HFen_HK
dc.date.accessioned2010-09-06T06:01:24Z-
dc.date.available2010-09-06T06:01:24Z-
dc.date.issued2009en_HK
dc.identifier.citationInternational Journal Of Cancer, 2009, v. 125 n. 11, p. 2631-2642en_HK
dc.identifier.issn0020-7136en_HK
dc.identifier.urihttp://hdl.handle.net/10722/68107-
dc.description.abstractOur previous study has suggested that the cell cycle-related kinase (CCRK) is a putative candidate oncogene in glioblastoma tumorigenesis. The potential oncogenic role of CCRK and its clinical/prognostic significance, however, in ovarian carcinoma are unclear. In this study, CCRK expression was examined by immunohistochemistry in a series of ovarian carcinoma tissues. Overexpression of CCRK was detected in 53% of the ovarian carcinomas, and it was positively correlated with an ascending histological grade and/or advanced clinical stage of the disease (p < 0.05). In addition, overexpression of CCRK in ovarian carcinoma was determined to be a strong and an independent predictor of short overall survival (p < 0.05). In ovarian carcinoma cells, CCRK knockdown by RNAi led to a G1 phase cell cycle arrest, while CCRK overexpression by stable transfection of CCRK-containing plasmid pcDNA-CCRK promoted cell proliferation in vitro and tumor growth in vivo. In addition, CCRK knockdown was found to reduce cyclin D1 expression. Consistently, CCRK overexpression increased cyclin D1 expression, and furthermore, a significant correlation between expression of CCRK and cyclin D1 in ovarian carcinomas was observed (p < 0.001). These findings suggest a potential important role of CCRK in the control of cell proliferation via regulation of cyclin D1 expression, and the overexpression of CCRK, as detected by immunohistochemistry, is an independent molecular marker for shortened survival time of patients with ovarian carcinoma. © 2009 UICC.en_HK
dc.languageengen_HK
dc.publisherJohn Wiley & Sons, Inc.. The Journal's web site is located at http://www3.interscience.wiley.com/journal/29331/homeen_HK
dc.relation.ispartofInternational Journal of Canceren_HK
dc.rightsInternational Journal of Cancer. Copyright © John Wiley & Sons, Inc.en_HK
dc.subjectCell cycleen_HK
dc.subjectCell cycle-related kinaseen_HK
dc.subjectCyclin D1en_HK
dc.subjectOvarian canceren_HK
dc.subjectPrognosisen_HK
dc.titleCell cycle-related kinase supports ovarian carcinoma cell proliferation via regulation of cyclin D1 and is a predictor of outcome in patients with ovarian carcinomaen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0020-7136&volume=125&spage=2631&epage=42&date=2009&atitle=Cell+cycle-related+kinase+supports+ovarian+carcinoma+cell+proliferation+via+regulation+of+cyclin+D1+and+is+a+predictor+of+outcome+in+patients+with+ovarian+carcinoma.en_HK
dc.identifier.emailGuan, XY:xyguan@hkucc.hku.hken_HK
dc.identifier.emailLin, MC:mcllin@hkucc.hku.hken_HK
dc.identifier.authorityGuan, XY=rp00454en_HK
dc.identifier.authorityLin, MC=rp00746en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1002/ijc.24630en_HK
dc.identifier.pmid19672860-
dc.identifier.scopuseid_2-s2.0-70350708151en_HK
dc.identifier.hkuros169985en_HK
dc.identifier.hkuros158790-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-70350708151&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume125en_HK
dc.identifier.issue11en_HK
dc.identifier.spage2631en_HK
dc.identifier.epage2642en_HK
dc.identifier.isiWOS:000271516500018-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridWu, GQ=7404976124en_HK
dc.identifier.scopusauthoridXie, D=35070710200en_HK
dc.identifier.scopusauthoridYang, GF=35082995900en_HK
dc.identifier.scopusauthoridLiao, YJ=36114448500en_HK
dc.identifier.scopusauthoridMai, SJ=36780688900en_HK
dc.identifier.scopusauthoridDeng, HX=24079601100en_HK
dc.identifier.scopusauthoridSze, J=7003867625en_HK
dc.identifier.scopusauthoridGuan, XY=7201463221en_HK
dc.identifier.scopusauthoridZeng, YX=7402981579en_HK
dc.identifier.scopusauthoridLin, MC=7404816359en_HK
dc.identifier.scopusauthoridKung, HF=7402514190en_HK

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