Evidence map›Paper›PMID 38003656›Full record

ArticleInternational journal of molecular sciences2023

RAR-Dependent and RAR-Independent RXR Signaling in Stem-like Glioma Cells.

Amanda Dabrock, Natalie Ernesti, Florian Will, Manaf Rana, Nadja Leinung, Phillip Ehrich, Volker Tronnier, Christina Zechel

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

Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.2field-weighted citation impact, top 40% 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

1 citing paper in PubMed, 1 citations in OpenAlex.

  1. 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

8 authors.

Amanda DabrockLaboratory of Experimental Neuro-Oncology, Center of Brain, Behavior and Metabolism, University Lübeck, Marie-Curie Strasse 66, D-23562 Lübeck, Germany.
Natalie ErnestiLaboratory of Experimental Neuro-Oncology, Center of Brain, Behavior and Metabolism, University Lübeck, Marie-Curie Strasse 66, D-23562 Lübeck, Germany.
Florian WillLaboratory of Experimental Neuro-Oncology, Center of Brain, Behavior and Metabolism, University Lübeck, Marie-Curie Strasse 66, D-23562 Lübeck, Germany.
Manaf RanaLaboratory of Experimental Neuro-Oncology, Center of Brain, Behavior and Metabolism, University Lübeck, Marie-Curie Strasse 66, D-23562 Lübeck, Germany.
Nadja LeinungLaboratory of Experimental Neuro-Oncology, Center of Brain, Behavior and Metabolism, University Lübeck, Marie-Curie Strasse 66, D-23562 Lübeck, Germany.
Phillip EhrichLaboratory of Experimental Neuro-Oncology, Center of Brain, Behavior and Metabolism, University Lübeck, Marie-Curie Strasse 66, D-23562 Lübeck, Germany.
Volker TronnierDepartment of Neurosurgery, University Clinic Schleswig-Holstein, Campus Lübeck, Ratzeburger Allee 160, D-23538 Lübeck, Germany.
Christina ZechelLaboratory of Experimental Neuro-Oncology, Center of Brain, Behavior and Metabolism, University Lübeck, Marie-Curie Strasse 66, D-23562 Lübeck, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Retinoic acid (RA) exerts pleiotropic effects during neural development and regulates homeostasis in the adult human brain. The RA signal may be transduced through RXR (retinoid-X receptor)-non-permissive RA receptor/RXR heterodimers or through RXR-permissive RXR heterodimers. The significance of RA signaling in malignant brain tumors such as glioblastoma multiforme (GBM) and gliosarcoma (GS) is poorly understood. In particular, the impact RA has on the proliferation, survival, differentiation, or metabolism of GBM- or GS-derived cells with features of stem cells (SLGCs) remains elusive. In the present manuscript, six GBM- and two GS-derived SLGC lines were analyzed for their responsiveness to RAR- and RXR-selective agonists. Inhibition of proliferation and initiation of differentiation were achieved with a RAR-selective pan-agonist in a subgroup of SLGC lines, whereas RXR-selective pan-agonists (rexinoids) supported proliferation in most SLGC lines. To decipher the RAR-dependent and RAR-independent effects of RXR, the genes encoding the RAR or RXR isotypes were functionally inactivated by CRISPR/Cas9-mediated editing in an IDH1-/p53-positive SLGC line with good responsiveness to RA. Stemness, differentiation capacity, and growth behavior were preserved after editing. Taken together, this manuscript provides evidence about the positive impact of RAR-independent RXR signaling on proliferation, survival, and tumor metabolism in SLGCs.

Indexed as

GliomaReceptors, Retinoic AcidAdultHumansRetinoidsRetinoid X ReceptorsStem CellsTretinoinReceptors, Retinoic AcidRetinoidsRetinoid X ReceptorsTretinoinCRISPR/Cas9 editingmalignant gliomaretinoic acid receptorsretinoid-X receptorsynthetic retinoids

Identifiers

PMID38003656
PMCPMC10671216
OpenAlexW4388761517

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.