File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Evaluation of nuclear factor-κB, urokinase-type plasminogen activator, and HBx and their clinicopathological significance in hepatocellular carcinoma

TitleEvaluation of nuclear factor-κB, urokinase-type plasminogen activator, and HBx and their clinicopathological significance in hepatocellular carcinoma
Authors
Issue Date2004
Citation
Clinical Cancer Research, 2004, v. 10 n. 12 I, p. 4140-4149 How to Cite?
AbstractPurpose: Nuclear factor κB (NF-κB) signaling pathway is an important regulating pathway in human diseases and cancers. One of its downstream target genes is urokinase plasminogen activator (uPA), which is involved in cancer invasion and metastasis. The purpose of this study was to evaluate NF-κB activation, uPA up-regulation, and hepatitis B viral X protein (HBx) expression in human hepatocellular carcinoma (HCC) and to assess their clinicopathological significance. Experimental Design: We evaluated NF-κB activation, expression of uPA, and presence of HBx in 32 human HCCs. Their clinicopathological significance was assessed by correlation with the clinicopathological features. Aberrant NF-κB signaling pathway and uPA up-regulation mediated by HBx were also analyzed in vitro. Results: We found that NF-κB activation and uPA up-regulation were frequently (56% and 59%, respectively) observed in HCCs, and particularly in HBx-positive HCCs. NF-κB activation and uPA overexpression were closely associated with one another (P < 0.0001). Furthermore, both activation of NF-κB and up-regulation of uPA were significantly associated with a more aggressive tumor behavior in terms of venous invasion, direct liver invasion, and absence of tumor encapsulation. In vitro, NF-κB activation was induced by HBx transfection in HepG2 cells through inhibitor of nuclear factor-κB kinase β (IKKβ). HBx also up-regulated uPA and enhanced cell invasion synergistically with IKKβ. Conclusions: The data indicate that NF-κB dysregulation and uPA overexpression may lead to a more aggressive tumor behavior in HCC. In addition, our data suggest that IKKβ plays a critical role in the HBx-activated NF-κB signaling pathway.
Persistent Identifierhttp://hdl.handle.net/10722/147530
ISSN
2015 Impact Factor: 8.738
2015 SCImago Journal Rankings: 5.314
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorChan, CFen_HK
dc.contributor.authorYau, TOen_HK
dc.contributor.authorJin, DYen_HK
dc.contributor.authorWong, CMen_HK
dc.contributor.authorFan, STen_HK
dc.contributor.authorNg, IOLen_HK
dc.date.accessioned2012-05-29T06:04:23Z-
dc.date.available2012-05-29T06:04:23Z-
dc.date.issued2004en_HK
dc.identifier.citationClinical Cancer Research, 2004, v. 10 n. 12 I, p. 4140-4149en_HK
dc.identifier.issn1078-0432en_HK
dc.identifier.urihttp://hdl.handle.net/10722/147530-
dc.description.abstractPurpose: Nuclear factor κB (NF-κB) signaling pathway is an important regulating pathway in human diseases and cancers. One of its downstream target genes is urokinase plasminogen activator (uPA), which is involved in cancer invasion and metastasis. The purpose of this study was to evaluate NF-κB activation, uPA up-regulation, and hepatitis B viral X protein (HBx) expression in human hepatocellular carcinoma (HCC) and to assess their clinicopathological significance. Experimental Design: We evaluated NF-κB activation, expression of uPA, and presence of HBx in 32 human HCCs. Their clinicopathological significance was assessed by correlation with the clinicopathological features. Aberrant NF-κB signaling pathway and uPA up-regulation mediated by HBx were also analyzed in vitro. Results: We found that NF-κB activation and uPA up-regulation were frequently (56% and 59%, respectively) observed in HCCs, and particularly in HBx-positive HCCs. NF-κB activation and uPA overexpression were closely associated with one another (P < 0.0001). Furthermore, both activation of NF-κB and up-regulation of uPA were significantly associated with a more aggressive tumor behavior in terms of venous invasion, direct liver invasion, and absence of tumor encapsulation. In vitro, NF-κB activation was induced by HBx transfection in HepG2 cells through inhibitor of nuclear factor-κB kinase β (IKKβ). HBx also up-regulated uPA and enhanced cell invasion synergistically with IKKβ. Conclusions: The data indicate that NF-κB dysregulation and uPA overexpression may lead to a more aggressive tumor behavior in HCC. In addition, our data suggest that IKKβ plays a critical role in the HBx-activated NF-κB signaling pathway.en_HK
dc.languageengen_US
dc.relation.ispartofClinical Cancer Researchen_HK
dc.subject.meshAdulten_US
dc.subject.meshAgeden_US
dc.subject.meshBlotting, Westernen_US
dc.subject.meshCarcinoma, Hepatocellular - Metabolismen_US
dc.subject.meshCell Line, Tumoren_US
dc.subject.meshCell Nucleus - Metabolismen_US
dc.subject.meshCytoplasm - Metabolismen_US
dc.subject.meshDna - Chemistryen_US
dc.subject.meshDna, Complementary - Metabolismen_US
dc.subject.meshFemaleen_US
dc.subject.meshGenes, Reporteren_US
dc.subject.meshHumansen_US
dc.subject.meshLiver - Pathologyen_US
dc.subject.meshLiver Neoplasms - Metabolismen_US
dc.subject.meshLuciferases - Metabolismen_US
dc.subject.meshMaleen_US
dc.subject.meshMiddle Ageden_US
dc.subject.meshNf-Kappa B - Biosynthesisen_US
dc.subject.meshNeoplasm Invasivenessen_US
dc.subject.meshNeoplasm Metastasisen_US
dc.subject.meshPlasmids - Metabolismen_US
dc.subject.meshPolymerase Chain Reactionen_US
dc.subject.meshRna - Metabolismen_US
dc.subject.meshRna, Messenger - Metabolismen_US
dc.subject.meshSignal Transductionen_US
dc.subject.meshTime Factorsen_US
dc.subject.meshTrans-Activators - Biosynthesisen_US
dc.subject.meshTransfectionen_US
dc.subject.meshUp-Regulationen_US
dc.subject.meshUrokinase-Type Plasminogen Activator - Biosynthesisen_US
dc.titleEvaluation of nuclear factor-κB, urokinase-type plasminogen activator, and HBx and their clinicopathological significance in hepatocellular carcinomaen_HK
dc.typeArticleen_HK
dc.identifier.emailJin, DY: dyjin@hkucc.hku.hken_HK
dc.identifier.emailWong, CM: jackwong@pathology.hku.hken_HK
dc.identifier.emailFan, ST: stfan@hku.hken_HK
dc.identifier.emailNg, IOL: iolng@hkucc.hku.hken_HK
dc.identifier.authorityJin, DY=rp00452en_HK
dc.identifier.authorityWong, CM=rp00231en_HK
dc.identifier.authorityFan, ST=rp00355en_HK
dc.identifier.authorityNg, IOL=rp00335en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1158/1078-0432.CCR-03-0574en_HK
dc.identifier.pmid15217951-
dc.identifier.scopuseid_2-s2.0-3042579870en_HK
dc.identifier.hkuros89302-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-3042579870&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume10en_HK
dc.identifier.issue12 Ien_HK
dc.identifier.spage4140en_HK
dc.identifier.epage4149en_HK
dc.identifier.isiWOS:000222249100030-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridChan, CF=7404814457en_HK
dc.identifier.scopusauthoridYau, TO=7006540669en_HK
dc.identifier.scopusauthoridJin, DY=7201973614en_HK
dc.identifier.scopusauthoridWong, CM=16314668400en_HK
dc.identifier.scopusauthoridFan, ST=7402678224en_HK
dc.identifier.scopusauthoridNg, IOL=7102753722en_HK

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats