Evidence map›Paper›PMID 18636537›Full record

ArticleJournal of cellular biochemistry2008

Blockage of NF-kappaB by IKKbeta- or RelA-siRNA rather than the NF-kappaB super-suppressor IkappaBalpha mutant potentiates adriamycin-induced cytotoxicity in lung cancer cells.

Wenshu Chen, Xia Wang, Lang Bai, Xiaomin Liang, Jianguo Zhuang, Yong Lin

Open access · greenAbstract read
In one paragraph

Article in Journal of cellular biochemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.5field-weighted citation impact, top 15% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

23 citing papers in PubMed, 42 citations in OpenAlex.

  1. Nuclear factor kappa B expression in non-small cell lung cancer.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2023
    Review
  2. Article
  3. Review
  4. Review
  5. Observational
  6. Review
  7. Repurposing of Bromocriptine for Cancer Therapy.Frontiers in pharmacology · 2018
    Article
  8. Pharmacogenomics of Scopoletin in Tumor Cells.Molecules (Basel, Switzerland) · 2016
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Nuclear factor-κB: a key regulator in health and disease of lungs.Archivum immunologiae et therapiae experimentalis · 2011
    Review
  19. Article
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Wenshu ChenMolecular Biology and Lung Cancer Program, Lovelace Respiratory Research Institute, Albuquerque, New Mexico 87108, USA.
Xia Wang
Lang Bai
Xiaomin Liang
Jianguo Zhuang
Yong Lin
Lovelace Respiratory Research Institute · US

Funding

Nutrient Flavonoids and Lung Cancer PreventionR03CA125796 · NCI · LOVELACE BIOMEDICAL & ENVIRONMENTAL RESEARCH INSTITUTE · PI LIN, YONG · 2007 to 2008
$205k
NCI NIH HHS R03 CA125796NCI NIH HHS R03CA125796
6 · The paper itself

Abstract

Ambiguous roles of genotoxic anticancer therapeutic-induced NF-kappaB activation in regulating gene expression (activation or suppression) and apoptosis (anti- or pro-apoptosis) have recently been suggested. In order to clarify this controversy and determine the usefulness of NF-kappaB blockage for sensitizing anticancer therapy, we have systematically investigated the effect of distinct NF-kappaB-blocking approaches on lung cancer cells' responses to Adriamycin-induced cytotoxicity. The results show that Adriamycin-induced NF-kappaB activation functions as a transcriptional activator triggering the expression of anti-apoptotic genes. Blocking NF-kappaB with IKKbeta- or RelA siRNA substantially sensitized Adriamycin-induced cytotoxicity, suggesting that the NF-kappaB pathway could be a target for sensitizing lung cancer cells to Adriamycin's anticancer effect. Surprisingly, although it effectively blocks NF-kappaB activation, the IkappaBalpha super-suppressor (IkappaBalphaAA) antagonized Adriamycin-induced cell death. Additionally, the induction of death receptor 5 (DR5), which contributes to Adriamycin-induced cytotoxicity, was not affected by NF-kappaB blockage. Thus, our results suggest that Adriamycin-induced NF-kappaB is a transcriptional activator that protects lung cancer cells against apoptosis, and IKKbeta- or RelA siRNA rather than IkappaBalphaAA is an appropriate NF-kappaB blocking approach for sensitizing lung cancer cells to Adriamycin-induced cytotoxicity.

Indexed as

ApoptosisCell Line, TumorDoxorubicinDrug Resistance, NeoplasmHumansI-kappa B KinaseI-kappa B ProteinsLung NeoplasmsMutationNF-kappa BNF-KappaB Inhibitor alphaRNA, Small InterferingTranscription Factor RelADoxorubicinI-kappa B KinaseI-kappa B ProteinsNF-kappa BNF-KappaB Inhibitor alphaNFKBIA protein, humanRELA protein, humanRNA, Small InterferingTranscription Factor RelA

Identifiers

PMID18636537
PMCPMC2688738
OpenAlexW2072346677

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.