Evidence map›Paper›PMID 31568628›Full record

ArticleJournal of cellular and molecular medicine2019

Non-lethal proteasome inhibition activates pro-tumorigenic pathways in multiple myeloma cells.

Aikaterini Skorda, Aimilia D Sklirou, Theodore Sakellaropoulos, Despoina D Gianniou, Efstathios Kastritis, Evangelos Terpos, Ourania E Tsitsilonis, Bogdan I Florea, Herman S Overkleeft, Meletios A Dimopoulos and 2 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of cellular and molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.5field-weighted citation impact, top 31% 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

4 citing papers in PubMed, 6 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. 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

12 authors at 3 institutions in 2 countries.

Aikaterini SkordaDepartment of Cell Biology and Biophysics, Faculty of Biology, National and Kapodistrian University of Athens, Athens, Greece.
Aimilia D SklirouDepartment of Cell Biology and Biophysics, Faculty of Biology, National and Kapodistrian University of Athens, Athens, Greece.
Theodore SakellaropoulosSchool of Mechanical Engineering, National Technical University of Athens, Athens, Greece.
Despoina D GianniouDepartment of Cell Biology and Biophysics, Faculty of Biology, National and Kapodistrian University of Athens, Athens, Greece.
Efstathios KastritisDepartment of Clinical Therapeutics, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece.
Evangelos TerposDepartment of Clinical Therapeutics, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece.
Ourania E TsitsilonisDepartment of Animal and Human Physiology, Faculty of Biology, National and Kapodistrian University of Athens, Athens, Greece.
Bogdan I FloreaGorlaeus Laboratories, Leiden Institute of Chemistry and Netherlands Proteomics Centre, Leiden, The Netherlands.
Herman S OverkleeftGorlaeus Laboratories, Leiden Institute of Chemistry and Netherlands Proteomics Centre, Leiden, The Netherlands.
Meletios A DimopoulosDepartment of Clinical Therapeutics, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece.
Leonidas G AlexopoulosSchool of Mechanical Engineering, National Technical University of Athens, Athens, Greece.
Ioannis P TrougakosDepartment of Cell Biology and Biophysics, Faculty of Biology, National and Kapodistrian University of Athens, Athens, Greece.ORCID 0000-0002-6179-2772
National and Kapodistrian University of Athens · GRNational Technical University of Athens · GRNetherlands Metabolomics Centre · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multiple myeloma (MM) is a haematological malignancy being characterized by clonal plasma cell proliferation in the bone marrow. Targeting the proteasome with specific inhibitors (PIs) has been proven a promising therapeutic strategy and PIs have been approved for the treatment of MM and mantle-cell lymphoma; yet, while outcome has improved, most patients inevitably relapse. As relapse refers to MM cells that survive therapy, we sought to identify the molecular responses induced in MM cells after non-lethal proteasome inhibition. By using bortezomib (BTZ), epoxomicin (EPOX; a carfilzomib-like PI) and three PIs, namely Rub999, PR671A and Rub1024 that target each of the three proteasome peptidases, we found that only BTZ and EPOX are toxic in MM cells at low concentrations. Phosphoproteomic profiling after treatment of MM cells with non-lethal (IC

Indexed as

Antineoplastic AgentsBone MarrowBortezomibCarcinogenesisCell Line, TumorCell SurvivalChemokine CXCL10HumansInterleukin-6Interleukin-8Multiple MyelomaOligopeptidesProteasome Endopeptidase ComplexProteasome InhibitorsProteomicsRecurrenceAntineoplastic AgentsBortezomibChemokine CXCL10epoxomicinIL6 protein, humanInterleukin-6Interleukin-8OligopeptidesProteasome Endopeptidase ComplexProteasome InhibitorsSTAT3 protein, humanSTAT3 Transcription FactorSTAT6 protein, humanSTAT6 Transcription Factorcytokineskinasesmultiple myelomaproteasomeproteasome inhibitors

Identifiers

PMID31568628
PMCPMC6850931
OpenAlexW2978147931

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.