Evidence map›Paper›PMID 23049692›Full record

ArticlePloS one2012

Role of Smad proteins in resistance to BMP-induced growth inhibition in B-cell lymphoma.

Kanutte Huse, Maren Bakkebø, Sébastien Wälchli, Morten P Oksvold, Vera I Hilden, Lise Forfang, May L Bredahl, Knut Liestøl, Ash A Alizadeh, Erlend B Smeland and 1 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

15 citing papers in PubMed, 20 citations in OpenAlex.

  1. BMP-ACVR1 Axis is Critical for Efficacy of PRC2 Inhibitors in B-Cell Lymphoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
  2. Article
  3. Expression and function of Smad7 in autoimmune and inflammatory diseases.Journal of molecular medicine (Berlin, Germany) · 2021
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. SMAD7: a timer of tumor progression targeting TGF-β signaling.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    Review
  12. Article
  13. Article
  14. Article
  15. Article
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

11 authors at 3 institutions in 2 countries.

Kanutte HuseSection of Immunology, Oslo University Hospital, Oslo, Norway. kanutte.huse@rr-research.no
Maren Bakkebø
Sébastien Wälchli
Morten P Oksvold
Vera I Hilden
Lise Forfang
May L Bredahl
Knut Liestøl
Ash A Alizadeh
Erlend B Smeland
June H Myklebust
Oslo University Hospital · NOUniversity of Oslo · NOStanford University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bone morphogenetic protein (BMP) expression and signaling are altered in a variety of cancers, but the functional impact of these alterations is uncertain. In this study we investigated the impact of expression of multiple BMPs and their signaling pathway components in human B-cell lymphoma. BMP messages, in particular BMP7, were detected in normal and malignant B cells. Addition of exogenous BMPs inhibited DNA synthesis in most lymphoma cell lines examined, but some cell lines were resistant. Tumor specimens from three out of five lymphoma patients were also resistant to BMPs, as determined by no activation of the BMP effectors Smad1/5/8. We have previously shown that BMP-7 potently induced apoptosis in normal B cells, which was in contrast to no or little inhibitory effect of this BMP in the lymphoma cells tested. BMP-resistance mechanisms were investigated by comparing sensitive and resistant cell lines. While BMP receptors are downregulated in many cancers, we documented similar receptor levels in resistant and sensitive lymphoma cells. We found a positive correlation between activation of Smad1/5/8 and inhibition of DNA synthesis. Gene expression analysis of two independent data sets showed that the levels of inhibitory Smads varied across different B-cell lymphoma. Furthermore, stable overexpression of Smad7 in two different BMP-sensitive cell lines with low endogenous levels of SMAD7, rendered them completely resistant to BMPs. This work highlights the role of Smads in determining the sensitivity to BMPs and shows that upregulation of Smad7 in cancer cells is sufficient to escape the negative effects of BMPs.

Indexed as

Amino Acid SequenceBlotting, WesternBone Morphogenetic ProteinsCell Line, TumorFlow CytometryGene Expression ProfilingGene Expression Regulation, NeoplasticHumansLymphoma, B-CellMolecular Sequence DataNucleic Acid Synthesis InhibitorsReal-Time Polymerase Chain ReactionReverse Transcriptase Polymerase Chain ReactionSignal TransductionSmad ProteinsBone Morphogenetic ProteinsNucleic Acid Synthesis InhibitorsSmad Proteins

Identifiers

PMID23049692
PMCPMC3462182
OpenAlexW2068290579

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.