File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: NF-κB protects rat ARL-6 hepatocellular carcinoma cells against hydrogen peroxide-induced apoptosis

TitleNF-κB protects rat ARL-6 hepatocellular carcinoma cells against hydrogen peroxide-induced apoptosis
Authors
KeywordsAdv-mIκBα
Apoptosis
Cell proliferation
Hepatocellular carcinoma (HCC) cell line
Hydrogen peroxide
Nuclear transcription factor-kappa B (NF-κB)
Oxidative stress
Primary rat hepatocyte culture
Issue Date2005
PublisherLandes Bioscience. The Journal's web site is located at http://www.landesbioscience.com/journals/cbt/index.php
Citation
Cancer Biology And Therapy, 2005, v. 4 n. 11, p. 1195-1202 How to Cite?
AbstractBackground/Aims: Refractoriness of some tumours to apoptosis has been related to over-expression of NF-κB, while NF-κB inhibition can promote apoptosis in several cell types. We compared NF-κB activation profiles between normal rat hepatocytes and ARL-6 rat hepatocellular carcinoma (HCC) cells exposed to hydrogen peroxide (H 2O 2), and examined whether NF-κB activation could explain the observed resistance to apoptosis of ARL-6 cells. We then infected ARL-6 cells with recombinant adenovirus containing mutant (non-degradable) IkBa (Adv-mIκBα), and examined whether this rendered ARL-6 cells more sensitive to oxidative stress-induced apoptosis. Methods: Cultured primary rat hepatocytes and ARL-6 cells were treated with graded doses of H 2O 2. To block NF-κB, ARL-6 cells were incubated with Adv-mIκBα for 24 h. Cytotoxicity, NF-κB activation, cell proliferation, and apoptosis were determined. Results: H 2O 2 induced more apoptosis in primary hepatocytes than ARL-6 cells, and the relative resistance of ARL-6 cells to H 2O 2-induced apoptosis was associated with more pronounced NF-κB activity. In ARL-6 cells, nuclear translocation of NF-κB took place within 2 h of administering H 2O 2 and remained prominent at 36 h. Adv-mIκBα sensitized ARL-6 cells to H 2O 2-induced apoptosis, but cell proliferation was minimally suppressed. Conclusions: Compared with normal hepatocytes, ARL-6 cells are refractory to apoptosis after exposure to H 2O 2, and this is associated with NF-κB activation. Conversely, NF-κB inhibition sensitises ARL-6 cells to H 2O 2-induced apoptosis. Sustained NF-κB activation in these HCC cells may protect them against apoptosis produced by oxidative stress. ©2005 Landes Bioscience.
Persistent Identifierhttp://hdl.handle.net/10722/78315
ISSN
2015 Impact Factor: 2.921
2015 SCImago Journal Rankings: 1.297
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorQiao, Len_HK
dc.contributor.authorYu, Jen_HK
dc.contributor.authorDent, Pen_HK
dc.contributor.authorFarrell, Gen_HK
dc.date.accessioned2010-09-06T07:41:31Z-
dc.date.available2010-09-06T07:41:31Z-
dc.date.issued2005en_HK
dc.identifier.citationCancer Biology And Therapy, 2005, v. 4 n. 11, p. 1195-1202en_HK
dc.identifier.issn1538-4047en_HK
dc.identifier.urihttp://hdl.handle.net/10722/78315-
dc.description.abstractBackground/Aims: Refractoriness of some tumours to apoptosis has been related to over-expression of NF-κB, while NF-κB inhibition can promote apoptosis in several cell types. We compared NF-κB activation profiles between normal rat hepatocytes and ARL-6 rat hepatocellular carcinoma (HCC) cells exposed to hydrogen peroxide (H 2O 2), and examined whether NF-κB activation could explain the observed resistance to apoptosis of ARL-6 cells. We then infected ARL-6 cells with recombinant adenovirus containing mutant (non-degradable) IkBa (Adv-mIκBα), and examined whether this rendered ARL-6 cells more sensitive to oxidative stress-induced apoptosis. Methods: Cultured primary rat hepatocytes and ARL-6 cells were treated with graded doses of H 2O 2. To block NF-κB, ARL-6 cells were incubated with Adv-mIκBα for 24 h. Cytotoxicity, NF-κB activation, cell proliferation, and apoptosis were determined. Results: H 2O 2 induced more apoptosis in primary hepatocytes than ARL-6 cells, and the relative resistance of ARL-6 cells to H 2O 2-induced apoptosis was associated with more pronounced NF-κB activity. In ARL-6 cells, nuclear translocation of NF-κB took place within 2 h of administering H 2O 2 and remained prominent at 36 h. Adv-mIκBα sensitized ARL-6 cells to H 2O 2-induced apoptosis, but cell proliferation was minimally suppressed. Conclusions: Compared with normal hepatocytes, ARL-6 cells are refractory to apoptosis after exposure to H 2O 2, and this is associated with NF-κB activation. Conversely, NF-κB inhibition sensitises ARL-6 cells to H 2O 2-induced apoptosis. Sustained NF-κB activation in these HCC cells may protect them against apoptosis produced by oxidative stress. ©2005 Landes Bioscience.en_HK
dc.languageengen_HK
dc.publisherLandes Bioscience. The Journal's web site is located at http://www.landesbioscience.com/journals/cbt/index.phpen_HK
dc.relation.ispartofCancer Biology and Therapyen_HK
dc.subjectAdv-mIκBαen_HK
dc.subjectApoptosisen_HK
dc.subjectCell proliferationen_HK
dc.subjectHepatocellular carcinoma (HCC) cell lineen_HK
dc.subjectHydrogen peroxideen_HK
dc.subjectNuclear transcription factor-kappa B (NF-κB)en_HK
dc.subjectOxidative stressen_HK
dc.subjectPrimary rat hepatocyte cultureen_HK
dc.titleNF-κB protects rat ARL-6 hepatocellular carcinoma cells against hydrogen peroxide-induced apoptosisen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1538-4047&volume=11&spage=1195&epage=202&date=2005&atitle=NF-κB+Protects+Rat+ARL-6+Hepatocellular+Carcinoma+Cells+Against+Hydrogen+Peroxide-Induced+Apoptosisen_HK
dc.identifier.emailQiao, L: lq8688@hotmail.comen_HK
dc.identifier.authorityQiao, L=rp00513en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.4161/cbt.4.11.2078-
dc.identifier.pmid16177566-
dc.identifier.scopuseid_2-s2.0-33645451985en_HK
dc.identifier.hkuros132370en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33645451985&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume4en_HK
dc.identifier.issue11en_HK
dc.identifier.spage1195en_HK
dc.identifier.epage1202en_HK
dc.identifier.isiWOS:000236044100013-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridQiao, L=7202151719en_HK
dc.identifier.scopusauthoridYu, J=35351306800en_HK
dc.identifier.scopusauthoridDent, P=7102148976en_HK
dc.identifier.scopusauthoridFarrell, G=7102979833en_HK

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats