ArticleOncogene2001
Increased and correlated nuclear factor-kappa B and Ku autoantigen activities are associated with development of multidrug resistance.
Article in Oncogene, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 46 citations in OpenAlex.
- Resveratrol induces AMPK-dependent MDR1 inhibition in colorectal cancer HCT116/L-OHP cells by preventing activation of NF-κB signaling and suppressing cAMP-responsive element transcriptional activity.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Article
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- Reversion of p-glycoprotein-mediated multidrug resistance in human leukemic cell line by diallyl trisulfide.Evidence-based complementary and alternative medicine : eCAM · 2012Article
- Disruption of microtubules sensitizes the DNA damage-induced apoptosis through inhibiting nuclear factor κB (NF-κB) DNA-binding activity.Journal of Korean medical science · 2010Article
- Helicobacter pylori in a Korean isolate expressed proteins differentially in human gastric epithelial cells.Digestive diseases and sciences · 2010Article
- In vitro anticancer property of a novel thalidomide analogue through inhibition of NF-kappaB activation in HL-60 cells.Acta pharmacologica Sinica · 2009Article
- Proteasome and NF-kappaB inhibiting phaeophytins from the green alga Cladophora fascicularis.Molecules (Basel, Switzerland) · 2007Article
- Role of nuclear factor-kappa B in melanoma.Cancer metastasis reviews · 2005Review
- Effects of the proteasome inhibitor bortezomib on osteolytic human prostate cancer cell metastases.Prostate cancer and prostatic diseases · 2005Article
- Identification of nucleophosmin as an NF-kappaB co-activator for the induction of the human SOD2 gene.The Journal of biological chemistry · 2004Article
- Article
- NF-kappaB transcription factor induces drug resistance through MDR1 expression in cancer cells.Oncogene · 2003Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In this study, we investigated possible engagement of NF-kappaB and Ku autoantigen (Ku) activation in development of multidrug resistance (MDR) and circumvention of MDR by modulation of NF-kappaB and Ku. The NF-kappaB activity and NF-kappaB p65 subunit level were constitutively higher in MDR cells than in drug-sensitive parental cells. Interestingly, a faster running NF-kappaB DNA binding complex was identified as Ku, a DNA damage sensor and a key double strand break repair protein, and was positively correlated with the NF-kappaB activity in MDR cells and Ku- or both subunits of NF-kappaB-transfected cells. Also both NF-kappaB and Ku activities were activated or inhibited by treatment with etoposide (VP-16) or MG-132 (a proteasome inhibitor), respectively. Furthermore, PKA inhibitor suppressed markedly the constitutive and drug-induced activities of NF-kappaB and Ku in MDR cells and subsequently potentiated the cytotoxic activity of anticancer drugs. Our results proposed that the NF-kappaB and Ku activation could be one of multi-factorial MDR mechanism, and PKA inhibitor, likely via inhibition of NF-kappaB and Ku activities, could enhance the effectiveness of anticancer drugs against MDR cells with high activities of NF-kappaB and Ku.
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