Evidence map›Paper›PMID 21063407›Full record

ArticleBritish journal of cancer2010

BH3-only protein Bik is involved in both apoptosis induction and sensitivity to oxidative stress in multiple myeloma.

L Bodet, E Ménoret, G Descamps, C Pellat-Deceunynck, R Bataille, S Le Gouill, P Moreau, M Amiot, P Gomez-Bougie

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

18 citing papers in PubMed, 31 citations in OpenAlex.

  1. A new era in cancer therapy: targeting the Proteasome-Bcl-2 axis.Journal of experimental & clinical cancer research : CR · 2025
    Review
  2. Mitochondrial dysfunction and drug targets in multiple myeloma.Journal of cancer research and clinical oncology · 2023
    Review
  3. Article
  4. Article
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  14. BCL-2 Antagonism to Target the Intrinsic Mitochondrial Pathway of Apoptosis.Clinical cancer research : an official journal of the American Association for Cancer Research · 2015
    Review
  15. Article
  16. Article
  17. Increase of novel biomarkers for oxidative stress in patients with plasma cell disorders and in multiple myeloma patients with bone lesions.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2012
    Article
  18. Metabolic stress in autophagy and cell death pathways.Cold Spring Harbor perspectives in biology · 2012
    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

9 authors at 3 institutions in 1 country.

L BodetInstitut de Recherche Thérapeutique de l'Université de Nantes, Equipe 10 labellisée Ligue Nationale contre le Cancer 2008, 8 quai Moncousu, Nantes BP70721 F-44007, France.
E Ménoret
G Descamps
C Pellat-Deceunynck
R Bataille
S Le Gouill
P Moreau
M Amiot
P Gomez-Bougie
Inserm · FRNantes Université · FRCentre d'Investigation Clinique de Nantes · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundalthough gene expression profile of multiple myeloma (MM) patients shows a wide range of Bik/Nbk expression, varying from absent to high, its regulation and function in myeloma cells is poorly understood. Thus, we addressed these questions in MM.

methodshuman myeloma cell lines (HMCLs) and primary purified myeloma cells were studied for Bcl-2 family protein expression by western blot and further correlation analysis was performed. Correlative study between Bik and thyrotroph embryonic factor (TEF) transcription factor expression was analysed by PCR. Stress oxidative response was analysed by flow cytometry.

resultsa strong expression of Bik protein was found only in one out of three of HMCL and correlated to Bcl-2 expression (P=0.0006). We demonstrated that Bik could be regulated at the protein level by Bcl-2 and at the transcriptional level by TEF. Bik overexpression sensitises myeloma cells to oxidative stress whereas Bik silencing increases resistance to H(2)O(2) oxidative stress. Furthermore, Bik ectopic expression disrupts Bim/Bcl-2 and Bim/Bcl-xL endogenous complexes triggering Bim release that could induce Bax and Bak activation.

conclusionsours results suggest that Bik has a role in both, apoptosis induction and sensitivity to oxidative stress in myeloma cells. Small BH3 mimetic molecules should be considered for further apoptosis-based therapy in myeloma cells expressing endogenous Bik/Bcl-2 complexes.

Indexed as

ApoptosisOxidative StressApoptosis Regulatory ProteinsBasic-Leucine Zipper Transcription FactorsHumansMembrane ProteinsMitochondrial ProteinsMultiple MyelomaProto-Oncogene Proteins c-bcl-2RNA, MessengerTumor Suppressor Protein p53Apoptosis Regulatory ProteinsBasic-Leucine Zipper Transcription FactorsBIK protein, humanMembrane ProteinsMitochondrial ProteinsProto-Oncogene Proteins c-bcl-2RNA, MessengerTEF protein, humanTumor Suppressor Protein p53

Identifiers

PMID21063407
PMCPMC3008608
OpenAlexW2014566849

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.