Evidence map›Paper›PMID 27286258›Full record

ArticleOncotarget2016

Cyclin D1 unbalances the redox status controlling cell adhesion, migration, and drug resistance in myeloma cells.

Sophie Bustany, Jérôme Bourgeais, Guergana Tchakarska, Simon Body, Olivier Hérault, Fabrice Gouilleux, Brigitte Sola

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.4field-weighted citation impact, top 17% 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

21 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Mitochondrial dysfunction and drug targets in multiple myeloma.Journal of cancer research and clinical oncology · 2023
    Review
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  7. Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. Review
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  14. Article
  15. Article
  16. Article
  17. Article
  18. Experimental and therapeutic medicine · 2018
    Article
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  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

7 authors at 4 institutions in 2 countries.

Sophie BustanyUniversité de Caen Normandie, EA4652 (MILPAT), MICAH Team, Caen, France.
Jérôme BourgeaisUniversité François Rabelais, CNRS UMR 7292 (GICC), LNOx Team, Tours, France.
Guergana TchakarskaUniversité de Caen Normandie, EA4652 (MILPAT), MICAH Team, Caen, France.
Simon BodyUniversité de Caen Normandie, EA4652 (MILPAT), MICAH Team, Caen, France.
Olivier HéraultUniversité François Rabelais, CNRS UMR 7292 (GICC), LNOx Team, Tours, France.
Fabrice GouilleuxUniversité François Rabelais, CNRS UMR 7292 (GICC), LNOx Team, Tours, France.
Brigitte SolaUniversité de Caen Normandie, EA4652 (MILPAT), MICAH Team, Caen, France.
Université de Caen Normandie · FRCentre National de la Recherche Scientifique · FRMcGill University Health Centre · CAUniversité de Tours · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The interactions of multiple myeloma (MM) cells with their microenvironment are crucial for pathogenesis. MM cells could interact differentially with their microenvironment depending on the type of cyclin D they express. We established several clones that constitutively express cyclin D1 from the parental RPMI8226 MM cell line and analyzed the impact of cyclin D1 expression on cell behavior. We performed a gene expression profiling study on cyclin D1-expressing vs. control cells and validated the results by semi-quantitative RT-PCR. The expression of cyclin D1 altered the transcription of genes that control adhesion and migration. We confirmed that cyclin D1 increases cell adhesion to stromal cells and fibronectin, stabilizes F-actin fibers, and enhances chemotaxis and inflammatory chemokine secretion. Both control and cyclin D1-expressing cells were more resistant to acute carfilzomib treatment when cultured on stromal cells than in suspension. However, this resistance was specifically reduced in cyclin D1-expressing cells after pomalidomide pre-treatment that modifies tumor cell/microenvironment interactions. Transcriptomic analysis revealed that cyclin D1 expression was also associated with changes in the expression of genes controlling metabolism. We also found that cyclin D1 expression disrupted the redox balance by producing reactive oxygen species. The resulting oxidative stress activated the p44/42 mitogen-activated protein kinase (or ERK1/2) signaling pathway, increased cell adhesion to fibronectin or stromal cells, and controlled drug sensitivity.Our results have uncovered a new function for cyclin D1 in the control of redox metabolism and interactions of cyclin D1-expressing MM cells with their bone marrow microenvironment.

Indexed as

Cell AdhesionCell Line, TumorCell MovementChemokinesCyclin D1Drug Resistance, NeoplasmExtracellular Signal-Regulated MAP KinasesHumansMultiple MyelomaOxidation-ReductionOxidative StressReactive Oxygen SpeciesThalidomideTumor MicroenvironmentCCND1 protein, humanChemokinesCyclin D1Extracellular Signal-Regulated MAP KinasespomalidomideReactive Oxygen SpeciesThalidomidecarfilzomibNADPH oxidasep44/42 mitogen-activated protein kinasepomalidomidereactive oxygen species

Identifiers

PMID27286258
PMCPMC5216717
OpenAlexW2415182610

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Registered trials

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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.