Evidence map›Paper›PMID 24116151›Full record

ArticlePloS one2013

Targeting neuroblastoma stem cells with retinoic acid and proteasome inhibitor.

Barbara Hämmerle, Yania Yañez, Sarai Palanca, Adela Cañete, Deborah J Burks, Victoria Castel, Jaime Font de Mora

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

39 citing papers in PubMed, 71 citations in OpenAlex.

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  17. Cancer stem cells in neuroblastoma therapy resistance.Cancer drug resistance (Alhambra, Calif.) · 2019
    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 1 country.

Barbara HämmerleLaboratory of Molecular Endocrinology, Centro de Investigación Príncipe Felipe, Valencia, Spain.
Yania Yañez
Sarai Palanca
Adela Cañete
Deborah J Burks
Victoria Castel
Jaime Font de Mora
Leitat Technological Center · ESCentro de Investigación Biomédica en Red Diabetes y Enfermedades Metabólicas Asociadas · ESCentro de Investigacion Principe Felipe · ESValencia Catholic University Saint Vincent Martyr · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNeuroblastma cell lines contain a side-population of cells which express stemness markers. These stem-like cells may represent the potential underlying mechanism for resistance to conventional therapy and recurrence of neuroblastoma in patients. METHODOLOGY/PRINCIPAL

findingsTo develop novel strategies for targeting the side-population of neurobastomas, we analyzed the effects of 13-cis-retinoic acid (RA) combined with the proteasome inhibitor MG132. The short-term action of the treatment was compared with effects after a 5-day recovery period during which both chemicals were withdrawn. RA induced growth arrest and differentiation of SH-SY5Y and SK-N-BE(2) neuroblastoma cell lines. Inhibition of the proteasome caused apoptosis in both cell lines, thus, revealing the critical role of this pathway in the regulated degradation of proteins involved in neuroblastoma proliferation and survival. The combination of RA with MG132 induced apoptosis in a dose-dependent manner, in addition to promoting G2/M arrest in treated cultures. Interestingly, expression of stem cell markers such as Nestin, Sox2, and Oct4 were reduced after the recovery period of combined treatment as compared with untreated cells or treated cells with either compound alone. Consistent with this, neurosphere formation was significantly impaired by the combined treatment of RA and MG132.

conclusionsGiven that stem-like cells are associated with resistant to conventional therapy and are thought to be responsible for relapse, our results suggest that dual therapy of RA and proteasome inhibitor might be beneficial for targeting the side-population of cells associated residual disease in high-risk neuroblastoma.

Indexed as

ApoptosisBlotting, WesternCell DifferentiationCell Line, TumorCell ProliferationDose-Response Relationship, DrugDrug SynergismFlow CytometryG2 Phase Cell Cycle CheckpointsHumansLeupeptinsMicroscopy, ConfocalNeoplastic Stem CellsNestinNeuroblastomaOctamer Transcription Factor-3benzyloxycarbonylleucyl-leucyl-leucine aldehydeLeupeptinsNES protein, humanNestinOctamer Transcription Factor-3POU5F1 protein, humanProteasome InhibitorsSOX2 protein, humanSOXB1 Transcription FactorsTretinoin

Identifiers

PMID24116151
PMCPMC3792090
OpenAlexW2067566186

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.