File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Activation of cyclin-dependent kinases CDC2 and CDK2 in hepatocellular carcinoma

TitleActivation of cyclin-dependent kinases CDC2 and CDK2 in hepatocellular carcinoma
Authors
KeywordsCell cycle
Cyclin
Cyclin-dependent kinase
Hepatocellular carcinoma
Liver
Issue Date2002
PublisherBlackwell Munksgaard. The Journal's web site is located at http://www.blackwellpublishing.com/journals/LIV
Citation
Liver, 2002, v. 22 n. 3, p. 259-268 How to Cite?
AbstractBackground: The cyclin-dependent kinases (CDKs) CDC2 and CDK2 are key regulators of the cell cycle. The expression of the CDK alone does not necessary reflect their true activities because they are highly regulated by post-translational mechanisms. Human hepatocellular carcinoma (HCC) is one of the most common cancers in the world, but the kinase activities of CDKs in HCC have not been examined. Methods: Here we examined the protein expression and kinase activities associated with CDC2 and CDK2 in HCC and the corresponding non-tumorous liver tissues. Results: CDC2 and CDK2 are activated in HCC in over 70% and 80% of the cases, respectively, but have little correlation with clinical parameters and PCNA expression. Interestingly, PCNA was readily detectable in extracts from non-tumorous liver, but more than 60% of samples contain higher concentration of PCNA in HCC than the corresponding non-tumorous tissues. CDC2 and CDK2 are generally activated in the same HCC samples, but the extent of their activation varied significantly, suggesting that the pathways leading to the activation of CDC2 and CDK2 can be regulated independently. Both positive regulators of CDK activity like cyclins and CDKs, and negative regulators of CDK activity like p21 CIPl/ WAF1 and Thrl 4/Tyr15 phosphorylation were up-regulated in HCC. Conclusion: CDC2 and CDK2 are activated in HCC, and this may be due to a complex interplay between the level of the cyclin, CDK, CDK inhibitors, and inhibitory phosphorylation.
Persistent Identifierhttp://hdl.handle.net/10722/88696
ISSN
2004 Impact Factor: 2.379
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLi, KKWen_HK
dc.contributor.authorNg, IOLen_HK
dc.contributor.authorFan, STen_HK
dc.contributor.authorAlbrecht, JHen_HK
dc.contributor.authorYamashita, Ken_HK
dc.contributor.authorPoon, RYCen_HK
dc.date.accessioned2010-09-06T09:46:46Z-
dc.date.available2010-09-06T09:46:46Z-
dc.date.issued2002en_HK
dc.identifier.citationLiver, 2002, v. 22 n. 3, p. 259-268en_HK
dc.identifier.issn0106-9543en_HK
dc.identifier.urihttp://hdl.handle.net/10722/88696-
dc.description.abstractBackground: The cyclin-dependent kinases (CDKs) CDC2 and CDK2 are key regulators of the cell cycle. The expression of the CDK alone does not necessary reflect their true activities because they are highly regulated by post-translational mechanisms. Human hepatocellular carcinoma (HCC) is one of the most common cancers in the world, but the kinase activities of CDKs in HCC have not been examined. Methods: Here we examined the protein expression and kinase activities associated with CDC2 and CDK2 in HCC and the corresponding non-tumorous liver tissues. Results: CDC2 and CDK2 are activated in HCC in over 70% and 80% of the cases, respectively, but have little correlation with clinical parameters and PCNA expression. Interestingly, PCNA was readily detectable in extracts from non-tumorous liver, but more than 60% of samples contain higher concentration of PCNA in HCC than the corresponding non-tumorous tissues. CDC2 and CDK2 are generally activated in the same HCC samples, but the extent of their activation varied significantly, suggesting that the pathways leading to the activation of CDC2 and CDK2 can be regulated independently. Both positive regulators of CDK activity like cyclins and CDKs, and negative regulators of CDK activity like p21 CIPl/ WAF1 and Thrl 4/Tyr15 phosphorylation were up-regulated in HCC. Conclusion: CDC2 and CDK2 are activated in HCC, and this may be due to a complex interplay between the level of the cyclin, CDK, CDK inhibitors, and inhibitory phosphorylation.en_HK
dc.languageengen_HK
dc.publisherBlackwell Munksgaard. The Journal's web site is located at http://www.blackwellpublishing.com/journals/LIVen_HK
dc.relation.ispartofLiveren_HK
dc.subjectCell cycleen_HK
dc.subjectCyclinen_HK
dc.subjectCyclin-dependent kinaseen_HK
dc.subjectHepatocellular carcinomaen_HK
dc.subjectLiveren_HK
dc.titleActivation of cyclin-dependent kinases CDC2 and CDK2 in hepatocellular carcinomaen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0106-9543&volume=22&spage=259&epage=268&date=2002&atitle=Activation+of+cyclin-dependent+kinases+CDC2+and+CDK2+in+hepatocellular+carcinomaen_HK
dc.identifier.emailNg, IOL: iolng@hkucc.hku.hken_HK
dc.identifier.emailFan, ST: stfan@hku.hken_HK
dc.identifier.authorityNg, IOL=rp00335en_HK
dc.identifier.authorityFan, ST=rp00355en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1046/j.0106-9543.2002.01629.xen_HK
dc.identifier.scopuseid_2-s2.0-0035990954en_HK
dc.identifier.hkuros77793en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0035990954&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume22en_HK
dc.identifier.issue3en_HK
dc.identifier.spage259en_HK
dc.identifier.epage268en_HK
dc.identifier.isiWOS:000176653700011-
dc.publisher.placeDenmarken_HK
dc.identifier.scopusauthoridLi, KKW=34971361400en_HK
dc.identifier.scopusauthoridNg, IOL=7102753722en_HK
dc.identifier.scopusauthoridFan, ST=7402678224en_HK
dc.identifier.scopusauthoridAlbrecht, JH=7202622750en_HK
dc.identifier.scopusauthoridYamashita, K=8854327800en_HK
dc.identifier.scopusauthoridPoon, RYC=7103097213en_HK

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats