File Download
  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Constitutive activation of NF-κB in human hepatocellular carcinoma: Evidence of a cytoprotective role

TitleConstitutive activation of NF-κB in human hepatocellular carcinoma: Evidence of a cytoprotective role
Authors
Issue Date2006
PublisherMary Ann Liebert, Inc. The Journal's web site is located at http://www.liebertpub.com/publication.aspx?pub_id=19&crit=Human%20Gene%20Therapy
Citation
Human Gene Therapy, 2006, v. 17 n. 3, p. 280-290 How to Cite?
AbstractActivation of nuclear factor-κB (NF-κB) can promote or inhibit apoptosis. Oxidative stress is an important mechanism by which certain anticancer drugs kill cancer cells, and is also one of the mechanisms that activate NF-κB. We therefore examined hepatic expression of the NF-κB monomer p65 in human hepatocellular carcinoma (HCC) tissue samples from eight patients and compared it with their respective samples of surrounding liver tissues. We also studied the effect of NF-κB inhibition in human HCC cells exposed to oxidative stress, by infecting HuH7 cells with a recombinant adenovirus carrying mutant IκBα (mIκBα). Cultured HuH7 cells were infected with mIκBα or β-galactosidase (β-Gal) for 24 hr followed by treatment with increasing concentrations of H2O2. Cytotoxicity, NF-κB translocation, NF-κB DNA binding, cell proliferation, and apoptosis were determined. The monomer p65 was overexpressed in six of eight human HCC tissues. In HuH7 cells, introduction of mIκBα potently inhibited the translocation, activation, and DNA binding of NF-κB. In control (β-Gal-infected) HuH7 cells, exposure to H2O2 produced a dose-dependent increase in apoptosis, regardless of NF-κB status. mIκBα- mediated inhibition of NF-κB activation sensitized HuH7 cells to H 2O2-induced inhibition of cell growth, and further promoted cell death. Addition of H2O2 (200-500 μM) to control or mIκBα-infected HuH7 cells enhanced caspase-3 activity and cleavage. Adenovirus-mediated transfer of mIκBα potently inhibits NF-κB activity in HuH7 cells, and this enhances oxidative stress-induced cell killing. © Mary Ann Liebert, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/76393
ISSN
2015 Impact Factor: 4.062
2015 SCImago Journal Rankings: 1.687
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorQiao, Len_HK
dc.contributor.authorZhang, Hen_HK
dc.contributor.authorYu, Jen_HK
dc.contributor.authorFrancisco, Ren_HK
dc.contributor.authorDent, Pen_HK
dc.contributor.authorEbert, MPAen_HK
dc.contributor.authorRöcken, Cen_HK
dc.contributor.authorFarrell, Gen_HK
dc.date.accessioned2010-09-06T07:20:45Z-
dc.date.available2010-09-06T07:20:45Z-
dc.date.issued2006en_HK
dc.identifier.citationHuman Gene Therapy, 2006, v. 17 n. 3, p. 280-290en_HK
dc.identifier.issn1043-0342en_HK
dc.identifier.urihttp://hdl.handle.net/10722/76393-
dc.description.abstractActivation of nuclear factor-κB (NF-κB) can promote or inhibit apoptosis. Oxidative stress is an important mechanism by which certain anticancer drugs kill cancer cells, and is also one of the mechanisms that activate NF-κB. We therefore examined hepatic expression of the NF-κB monomer p65 in human hepatocellular carcinoma (HCC) tissue samples from eight patients and compared it with their respective samples of surrounding liver tissues. We also studied the effect of NF-κB inhibition in human HCC cells exposed to oxidative stress, by infecting HuH7 cells with a recombinant adenovirus carrying mutant IκBα (mIκBα). Cultured HuH7 cells were infected with mIκBα or β-galactosidase (β-Gal) for 24 hr followed by treatment with increasing concentrations of H2O2. Cytotoxicity, NF-κB translocation, NF-κB DNA binding, cell proliferation, and apoptosis were determined. The monomer p65 was overexpressed in six of eight human HCC tissues. In HuH7 cells, introduction of mIκBα potently inhibited the translocation, activation, and DNA binding of NF-κB. In control (β-Gal-infected) HuH7 cells, exposure to H2O2 produced a dose-dependent increase in apoptosis, regardless of NF-κB status. mIκBα- mediated inhibition of NF-κB activation sensitized HuH7 cells to H 2O2-induced inhibition of cell growth, and further promoted cell death. Addition of H2O2 (200-500 μM) to control or mIκBα-infected HuH7 cells enhanced caspase-3 activity and cleavage. Adenovirus-mediated transfer of mIκBα potently inhibits NF-κB activity in HuH7 cells, and this enhances oxidative stress-induced cell killing. © Mary Ann Liebert, Inc.en_HK
dc.languageengen_HK
dc.publisherMary Ann Liebert, Inc. The Journal's web site is located at http://www.liebertpub.com/publication.aspx?pub_id=19&crit=Human%20Gene%20Therapyen_HK
dc.relation.ispartofHuman Gene Therapyen_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.rightsThis is a copy of an article published in the [Human Gene Therapy] © [2006] [copyright Mary Ann Liebert, Inc.]; [Human Gene Therapy] is available online at: http://www.liebertonline.com.-
dc.titleConstitutive activation of NF-κB in human hepatocellular carcinoma: Evidence of a cytoprotective roleen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1043-0342&volume=17&spage=280&epage=290&date=2006&atitle=Constitutive+Activation+of+NF-κB+in+Human+Hepatocellular+Carcinoma:+Evidence+of+a+Cytoprotective+Roleen_HK
dc.identifier.emailQiao, L: qiaol@hkucc.hku.hken_HK
dc.identifier.authorityQiao, L=rp00513en_HK
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1089/hum.2006.17.280en_HK
dc.identifier.pmid16544977-
dc.identifier.scopuseid_2-s2.0-33645457576en_HK
dc.identifier.hkuros132308en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33645457576&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume17en_HK
dc.identifier.issue3en_HK
dc.identifier.spage280en_HK
dc.identifier.epage290en_HK
dc.identifier.isiWOS:000236225800003-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridQiao, L=7202151719en_HK
dc.identifier.scopusauthoridZhang, H=7409191451en_HK
dc.identifier.scopusauthoridYu, J=35351306800en_HK
dc.identifier.scopusauthoridFrancisco, R=12798233200en_HK
dc.identifier.scopusauthoridDent, P=7102148976en_HK
dc.identifier.scopusauthoridEbert, MPA=35239660600en_HK
dc.identifier.scopusauthoridRöcken, C=7006367084en_HK
dc.identifier.scopusauthoridFarrell, G=7102979833en_HK

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats