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Article: Characterization of the oncogenic function of centromere protein F in hepatocellular carcinoma

TitleCharacterization of the oncogenic function of centromere protein F in hepatocellular carcinoma
Authors
Issue Date2013
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/wps/find/journaldescription.cws_home/622790/description
Citation
Biochemical and Biophysical Research Communications, 2013, v. 436 n. 4, p. 711-718 How to Cite?
AbstractCentromere protein F (CENPF) is an essential nuclear protein associated with the centromere-kinetochore complex and plays a critical role in chromosome segregation during mitosis. Up-regulation of CENPF expression has previously been detected in several solid tumors. In this study, we aim to study the expression and functional role of CENPF in hepatocellular carcinoma (HCC). We found CENPF was frequently overexpressed in HCC as compared with non-tumor tissue. Up-regulated CENPF expression in HCC was positively correlated with serum AFP, venous invasion, advanced differentiation stage and a shorter overall survival. Cox regression analysis found that overexpression of CENPF was an independent prognosis factor in HCC. Functional studies found that silencing CENPF could decrease the ability of the cells to proliferate, form colonies and induce tumor formation in nude mice. Silencing CENPF also resulted in the cell cycle arrest at G2/M checkpoint by down-regulating cell cycle proteins cdc2 and cyclin B1. Our data suggest that CENPF is frequently overexpressed in HCC and plays a critical role in driving HCC tumorigenesis. © 2013 Elsevier Inc.
Persistent Identifierhttp://hdl.handle.net/10722/184489
ISSN
2015 Impact Factor: 2.371
2015 SCImago Journal Rankings: 1.152
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorDai, YD-
dc.contributor.authorLiu, LL-
dc.contributor.authorZeng, TT-
dc.contributor.authorZhu, YH-
dc.contributor.authorLi, JC-
dc.contributor.authorChen, L-
dc.contributor.authorLi, Y-
dc.contributor.authorYuan, YF-
dc.contributor.authorMa, SKY-
dc.contributor.authorGuan, X-
dc.date.accessioned2013-07-15T09:50:25Z-
dc.date.available2013-07-15T09:50:25Z-
dc.date.issued2013-
dc.identifier.citationBiochemical and Biophysical Research Communications, 2013, v. 436 n. 4, p. 711-718-
dc.identifier.issn0006-291X-
dc.identifier.urihttp://hdl.handle.net/10722/184489-
dc.description.abstractCentromere protein F (CENPF) is an essential nuclear protein associated with the centromere-kinetochore complex and plays a critical role in chromosome segregation during mitosis. Up-regulation of CENPF expression has previously been detected in several solid tumors. In this study, we aim to study the expression and functional role of CENPF in hepatocellular carcinoma (HCC). We found CENPF was frequently overexpressed in HCC as compared with non-tumor tissue. Up-regulated CENPF expression in HCC was positively correlated with serum AFP, venous invasion, advanced differentiation stage and a shorter overall survival. Cox regression analysis found that overexpression of CENPF was an independent prognosis factor in HCC. Functional studies found that silencing CENPF could decrease the ability of the cells to proliferate, form colonies and induce tumor formation in nude mice. Silencing CENPF also resulted in the cell cycle arrest at G2/M checkpoint by down-regulating cell cycle proteins cdc2 and cyclin B1. Our data suggest that CENPF is frequently overexpressed in HCC and plays a critical role in driving HCC tumorigenesis. © 2013 Elsevier Inc.-
dc.languageeng-
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/wps/find/journaldescription.cws_home/622790/description-
dc.relation.ispartofBiochemical and Biophysical Research Communications-
dc.titleCharacterization of the oncogenic function of centromere protein F in hepatocellular carcinoma-
dc.typeArticle-
dc.identifier.emailChen, L: pollyllc@hku.hk-
dc.identifier.emailMa, SKY: stefma@hku.hk-
dc.identifier.emailGuan, X: xyguan@hkucc.hku.hk-
dc.identifier.authorityMa, SKY=rp00506-
dc.identifier.authorityGuan, X=rp00454-
dc.identifier.doi10.1016/j.bbrc.2013.06.021-
dc.identifier.pmid23791740-
dc.identifier.scopuseid_2-s2.0-84880041768-
dc.identifier.hkuros215086-
dc.identifier.volume436-
dc.identifier.issue4-
dc.identifier.spage711-
dc.identifier.epage718-
dc.identifier.isiWOS:000322415400025-
dc.publisher.placeUnited States-

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