Evidence map›Paper›PMID 28420882›Full record

ArticleScientific reports2017

The role of the SWI/SNF chromatin remodeling complex in maintaining the stemness of glioma initiating cells.

Hiroaki Hiramatsu, Kazuyoshi Kobayashi, Kyousuke Kobayashi, Takeshi Haraguchi, Yasushi Ino, Tomoki Todo, Hideo Iba

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

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

25 citing papers in PubMed, 41 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Hiroaki HiramatsuDivision of Host-Parasite Interaction, Department of Microbiology and Immunology, The Institute of Medical Science, The University of Tokyo, Tokyo, 108-8639, Japan.
Kazuyoshi KobayashiDivision of Host-Parasite Interaction, Department of Microbiology and Immunology, The Institute of Medical Science, The University of Tokyo, Tokyo, 108-8639, Japan.
Kyousuke KobayashiDivision of Host-Parasite Interaction, Department of Microbiology and Immunology, The Institute of Medical Science, The University of Tokyo, Tokyo, 108-8639, Japan.
Takeshi HaraguchiDivision of Host-Parasite Interaction, Department of Microbiology and Immunology, The Institute of Medical Science, The University of Tokyo, Tokyo, 108-8639, Japan.
Yasushi InoDivision of Innovative Cancer Therapy, and Department of Surgical Neuro-Oncology, The Institute of Medical Science, The University of Tokyo, Tokyo, 108-8639, Japan.ORCID http://orcid.org/0000-0002-2609-1962
Tomoki TodoDivision of Innovative Cancer Therapy, and Department of Surgical Neuro-Oncology, The Institute of Medical Science, The University of Tokyo, Tokyo, 108-8639, Japan.
Hideo IbaDivision of Host-Parasite Interaction, Department of Microbiology and Immunology, The Institute of Medical Science, The University of Tokyo, Tokyo, 108-8639, Japan. iba@ims.u-tokyo.ac.jp.
Chiba University Hospital · JPThe University of Tokyo · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioma initiating cells (GICs) are thought to contribute to therapeutic resistance and tumor recurrence in glioblastoma, a lethal primary brain tumor in adults. Although the stem-like properties of GICs, such as self-renewal and tumorigenicity, are epigenetically regulated, the role of a major chromatin remodeling complex in human, the SWI/SNF complex, remains unknown in these cells. We here demonstrate that the SWI/SNF core complex, that is associated with a unique corepressor complex through the d4-family proteins, DPF1 or DPF3a, plays essential roles in stemness maintenance in GICs. The serum-induced differentiation of GICs downregulated the endogenous expression of DPF1 and DPF3a, and the shRNA-mediated knockdown of each gene reduced both sphere-forming ability and tumor-forming activity in a mouse xenograft model. Rescue experiments revealed that DPF1 has dominant effects over DPF3a. Notably, whereas we have previously reported that d4-family members can function as adaptor proteins between the SWI/SNF complex and NF-κB dimers, this does not significantly contribute to maintaining the stemness properties of GICs. Instead, these proteins were found to link a corepressor complex containing the nuclear receptor, TLX, and LSD1/RCOR2 with the SWI/SNF core complex. Collectively, our results indicate that DPF1 and DPF3a are potential therapeutic targets for glioblastoma.

Indexed as

Chromatin Assembly and DisassemblyCells, CulturedChromosomal Proteins, Non-HistoneCo-Repressor ProteinsDNA-Binding ProteinsGene Expression Regulation, NeoplasticGliomaHumansNeoplastic Stem CellsNerve Tissue ProteinsNF-kappa BOrphan Nuclear ReceptorsReceptors, Cytoplasmic and NuclearTranscription FactorsChromosomal Proteins, Non-HistoneCo-Repressor ProteinsDNA-Binding ProteinsDPF1 protein, humanDPF3 protein, humanNerve Tissue ProteinsNF-kappa BNR2E1 protein, humanOrphan Nuclear ReceptorsRcor2 protein, humanReceptors, Cytoplasmic and NuclearSWI-SNF-B chromatin-remodeling complexTranscription Factors

Identifiers

PMID28420882
PMCPMC5429847
OpenAlexW2606339667

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.