Evidence map›Paper›PMID 19503092›Full record

ArticleOncogene2009

Cyclophilins contribute to Stat3 signaling and survival of multiple myeloma cells.

K Bauer, A K Kretzschmar, H Cvijic, C Blumert, D Löffler, K Brocke-Heidrich, C Schiene-Fischer, G Fischer, A Sinz, C V Clevenger and 1 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.9field-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

28 citing papers in PubMed, 65 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Non-Immunosuppressive Cyclophilin Inhibitors.Angewandte Chemie (International ed. in English) · 2022
    Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Secreted cyclophilin A mediates G1/S phase transition of cholangiocarcinoma cells via CD147/ERK1/2 pathway.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
    Article
  17. Article
  18. Article
  19. Article
  20. HAb18G/CD147 promotes pSTAT3-mediated pancreatic cancer development via CD44s.Clinical cancer research : an official journal of the American Association for Cancer Research · 2013
    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 4 institutions in 2 countries.

K BauerInstitute of Clinical Immunology and Transfusion Medicine, University of Leipzig, Germany.
A K Kretzschmar
H Cvijic
C Blumert
D Löffler
K Brocke-Heidrich
C Schiene-Fischer
G Fischer
A Sinz
C V Clevenger
F Horn
Leipzig University · DEMax Planck Research Unit for Enzymology of Protein Folding · DEMartin Luther University Halle-Wittenberg · DENorthwestern University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Signal transducer and activator of transcription 3 (Stat3) is the major mediator of interleukin-6 (IL-6) family cytokines. In addition, Stat3 is known to be involved in the pathophysiology of many malignancies. Here, we show that the cis-trans peptidyl-prolyl isomerase cyclophilin (Cyp) B specifically interacts with Stat3, whereas the highly related CypA does not. CypB knockdown inhibited the IL-6-induced transactivation potential but not the tyrosine phosphorylation of Stat3. Binding of CypB to Stat3 target promoters and alteration of the intranuclear localization of Stat3 on CypB depletion suggested a nuclear function of Stat3/CypB interaction. By contrast, CypA knockdown inhibited Stat3 IL-6-induced tyrosine phosphorylation and nuclear translocation. The Cyp inhibitor cyclosporine A (CsA) caused similar effects. However, Stat1 activation in response to IL-6 or interferon-gamma was not affected by Cyp silencing or CsA treatment. As a result, Cyp knockdown shifted IL-6 signaling to a Stat1-dominated pathway. Furthermore, Cyp depletion or treatment with CsA induced apoptosis in IL-6-dependent multiple myeloma cells, whereas an IL-6-independent line was not affected. Thus, Cyps support the anti-apoptotic action of Stat3. Taken together, CypA and CypB both play pivotal roles, yet at different signaling levels, for Stat3 activation and function. These data also suggest a novel mechanism of CsA action.

Indexed as

Signal TransductionApoptosisCell CycleCell LineCell Line, TumorCell SurvivalChromatin ImmunoprecipitationCyclophilin ACyclophilinsFlow CytometryHumansImmunoblottingInterleukin-6LuciferasesLuminescent ProteinsMicroscopy, FluorescenceCyclophilin Acyclophilin BCyclophilinsInterleukin-6LuciferasesLuminescent ProteinsRecombinant Fusion ProteinsRNA, Small InterferingSTAT3 Transcription Factor

Identifiers

PMID19503092
OpenAlexW2083019799

What OpenQuestion holds

Textmetadata
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.