Evidence map›Paper›PMID 28925404›Full record

ArticleOncogene2018

ING5 activity in self-renewal of glioblastoma stem cells via calcium and follicle stimulating hormone pathways.

F Wang, A Y Wang, C Chesnelong, Y Yang, A Nabbi, S Thalappilly, V Alekseev, K Riabowol

Open access · hybridAbstract read
In one paragraph

Article in Oncogene, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

27 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
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  9. Review
  10. Tctp, a unique Ing5-binding partner, inhibits the chromatin binding of Enok inProceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  11. Article
  12. Review
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  15. Article
  16. The roles of ING5 in cancer: A tumor suppressor.Frontiers in cell and developmental biology · 2022
    Review
  17. Article
  18. Review
  19. Article
  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

8 authors at 2 institutions in 2 countries.

F WangDepartment of Biochemistry & Molecular Biology, University of Calgary, Calgary, AB, Canada.
A Y WangDepartment of Oncology, Arnie Charbonneau Cancer Institute, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada.
C ChesnelongDepartment of Oncology, Arnie Charbonneau Cancer Institute, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada.
Y YangDepartment of Biochemistry & Molecular Biology, University of Calgary, Calgary, AB, Canada.
A NabbiDepartment of Biochemistry & Molecular Biology, University of Calgary, Calgary, AB, Canada.
S ThalappillyDepartment of Biochemistry & Molecular Biology, University of Calgary, Calgary, AB, Canada.
V AlekseevDepartment of Biochemistry & Molecular Biology, University of Calgary, Calgary, AB, Canada.
K RiabowolDepartment of Biochemistry & Molecular Biology, University of Calgary, Calgary, AB, Canada.
University of Calgary · CAHarbin Medical University · CN

Funding

CIHR MOP-133646
6 · The paper itself

Abstract

Stem cell-like brain tumor initiating cells (BTICs) cause recurrence of glioblastomas, with BTIC 'stemness' affected by epigenetic mechanisms. The ING family of epigenetic regulators (ING1-5) function by targeting histone acetyltransferase (HAT) or histone deacetylase complexes to the H3K4me3 mark to alter histone acetylation and subsequently, gene expression. Here we find that ectopic expression of ING5, the targeting subunit of HBO1, MOZ and MORF HAT complexes increases expression of the Oct4, Olig2 and Nestin stem cell markers, promotes self-renewal, prevents lineage differentiation and increases stem cell pools in BTIC populations. This activity requires the plant homeodomain region of ING5 that interacts specifically with the H3K4me3 mark. ING5 also enhances PI3K/AKT and MEK/ERK activity to sustain self-renewal of BTICs over serial passage of stem cell-like spheres. ING5 exerts these effects by activating transcription of calcium channel and follicle stimulating hormone pathway genes. In silico analyses of The Cancer Genome Atlas data suggest that ING5 is a positive regulator of BTIC stemness, whose expression negatively correlates with patient prognosis, especially in the Proneural and Classical subtypes, and in tumors with low SOX2 expression. These data suggest that altering histone acetylation status and signaling pathways induced by ING5 may provide useful clinical strategies to target tumor resistance and recurrence in glioblastoma.

Indexed as

AcetylationAdultBrainBrain NeoplasmsCalciumCell Line, TumorComputer SimulationFollicle Stimulating HormoneGene Expression Regulation, NeoplasticGlioblastomaHistone AcetyltransferasesHistonesHumansKaplan-Meier EstimateNeoplasm Recurrence, LocalNeoplastic Stem CellsCalciumFollicle Stimulating HormoneHistone AcetyltransferasesHistonesING5 protein, humanSOX2 protein, humanSOXB1 Transcription FactorsTranscription FactorsTumor Suppressor Proteins

Identifiers

PMID28925404
PMCPMC5799773
OpenAlexW2753952998

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.