Evidence map›Paper›PMID 27434731›Full record

ArticleCancer biology & therapy2016

Bruceantin inhibits multiple myeloma cancer stem cell proliferation.

Mark E Issa, Sarah Berndt, Gilles Carpentier, John M Pezzuto, Muriel Cuendet

Open access · bronzeAbstract read
In one paragraph

Article in Cancer biology & therapy, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

17 citing papers in PubMed, 35 citations in OpenAlex.

  1. Review
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  5. A Comprehensive Look at In Vitro Angiogenesis Image Analysis Software.International journal of molecular sciences · 2023
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  6. Review
  7. Article
  8. A Concise Enantioselective Approach to Quassinoids.Journal of the American Chemical Society · 2022
    Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Future in the Past:International journal of molecular sciences · 2018
    Article
  16. Article
  17. 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

5 authors at 4 institutions in 3 countries.

Mark E Issaa School of Pharmaceutical Sciences , University of Geneva, University of Lausanne, Rue Michel Servet , Geneva , Switzerland.
Sarah Berndta School of Pharmaceutical Sciences , University of Geneva, University of Lausanne, Rue Michel Servet , Geneva , Switzerland.
Gilles Carpentierb Laboratoire CRRET, Faculté des Sciences et Technologie , Université Paris Est Créteil , Créteil Cedex , France.
John M Pezzutoc Arnold & Marie Schwartz College of Pharmacy and Health Sciences , Long Island University , Brooklyn , NY , USA.
Muriel Cuendeta School of Pharmaceutical Sciences , University of Geneva, University of Lausanne, Rue Michel Servet , Geneva , Switzerland.
University of Geneva · CHLong Island University · USUniversité Paris-Est Créteil · FRUniversity of Lausanne · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multiple myeloma (MM) continues to claim the lives of a majority of patients. MM cancer stem cells (CSCs) have been demonstrated to sustain tumor growth. Due to their ability to self-renew and to express detoxifying enzymes and efflux transporters, MM-CSCs are rendered highly resistant to conventional therapies. Therefore, managing MM-CSCs characteristics could have profound clinical implications. Bruceantin (BCT) is a natural product previously demonstrated to inhibit the growth of MM in RPMI 8226 cells-inoculated mouse xenograft models, and to cause regression in already established tumors. The objectives of the present study were to test the inhibitory effects of BCT on MM-CSCs growth derived from a human primary tumor, and to explore a mechanism of action underlying these effects. BCT exhibited potent antiproliferative activity in MM-CSCs starting at 25 nM. BCT induced cell cycle arrest, cell death and apoptosis in MM-CSCs as well as inhibited cell migration and angiogenesis in vitro. Using a qPCR screen, it was found that the gene expression of a number of Notch pathway members was altered. Pretreatment of MM-CSCs with the γ-secretase inhibitor RO4929097, a Notch pathway inhibitor, reversed BCT-induced effects on MM-CSCs proliferation. In this study, BCT was shown to be an effective agent in controlling the proliferation, viability and migration of MM-CSCs as well as angiogenesis in vitro. The effect on MM-CSCs proliferation may be mediated by the Notch pathway. These results warrant further investigation of BCT in a broader set of human-derived MM-CSCs and with in vivo models representative of MM.

Indexed as

Antineoplastic Agents, PhytogenicCell ProliferationHumansHuman Umbilical Vein Endothelial CellsMultiple MyelomaNeoplastic Stem CellsQuassinsAntineoplastic Agents, PhytogenicbruceantinQuassinsBruceantincancer stem cellscell deathmultiple myelomanotchproliferation

Identifiers

PMID27434731
PMCPMC5036415
OpenAlexW2499386581

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.