Evidence map›Paper›PMID 32492707›Full record

ArticleNeuro-oncology2020

TRIM24 promotes stemness and invasiveness of glioblastoma cells via activating Sox2 expression.

Lu-Hua Zhang, Yi-Heng Yin, Hong-Zun Chen, Shi-Yu Feng, Jia-Lin Liu, Ling Chen, Wen-Liang Fu, Guo-Chen Sun, Xin-Guang Yu, Dong-Gang Xu

Open access · bronzeAbstract read
In one paragraph

Article in Neuro-oncology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing 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

32 citing papers in PubMed, 51 citations in OpenAlex.

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  18. C-Fos-activated circRPPH1 contributes to glioma stemness.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023
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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

10 authors at 2 institutions in 1 country.

Lu-Hua ZhangDepartment of Neurosurgery, the First Medical Center, Chinese PLA General Hospital, Beijing, China.
Yi-Heng YinDepartment of Neurosurgery, the First Medical Center, Chinese PLA General Hospital, Beijing, China.
Hong-Zun ChenDepartment of Neurosurgery, the Second Hospital of PLA Southern Navy, Sanya, Hainan, China.
Shi-Yu FengDepartment of Neurosurgery, the First Medical Center, Chinese PLA General Hospital, Beijing, China.
Jia-Lin LiuDepartment of Neurosurgery, the First Medical Center, Chinese PLA General Hospital, Beijing, China.
Ling ChenDepartment of Neurosurgery, the First Medical Center, Chinese PLA General Hospital, Beijing, China.
Wen-Liang FuInstitute of Military Cognitive and Brain Sciences, Academy of Military Medical Sciences, Beijing, China.
Guo-Chen SunDepartment of Neurosurgery, the First Medical Center, Chinese PLA General Hospital, Beijing, China.
Xin-Guang YuDepartment of Neurosurgery, the First Medical Center, Chinese PLA General Hospital, Beijing, China.
Dong-Gang XuInstitute of Military Cognitive and Brain Sciences, Academy of Military Medical Sciences, Beijing, China.
Chinese PLA General Hospital · CNAcademy of Military Medical Sciences · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGlioblastoma stem cells (GSCs) are a subpopulation of glioblastoma (GBM) cells that are critical for tumor invasion and treatment resistance. However, little is known about the function and mechanism of tripartite motif-containing 24 (TRIM24) in GSCs.

methodsImmunofluorescence, flow cytometry, and western blot analyses were used to evaluate TRIM24 and cluster of differentiation (CD)133 expression profiles in GBM surgical specimens and GSC tumorspheres. Different TRIM24 expression levels in patients' tumors, as measured by both immunohistochemistry and western blot, were related to their corresponding MRI data. Wound healing, Matrigel invasion, and xenograft immunohistochemistry were conducted to determine GBM cell invasion.

resultsWe identified that TRIM24 was coexpressed with CD133 and Nestin in GBM tissues and tumorsphere cells. Limiting dilution assays and xenotransplantation experiments illustrated that knockdown of TRIM24 expression reduced GSC self-renewal capacity and invasive growth. TRIM24 expression levels were positively associated with the volumes of peritumoral T2 weighted image abnormality. Rescue experiments indicated TRIM24 participation in GBM infiltrative dissemination. Chromatin immunoprecipitation, reporter gene assay, PCR, western blot, and immunohistochemistry demonstrated that TRIM24 activated the expression of the pluripotency transcription factor sex determining region Y-box 2 (Sox2) to regulate GBM stemness and invasion in vitro and in vivo. Finally, the close relationship between TRIM24 and Sox2 was validated by testing samples enrolled in our study and exploring external databases.

conclusionsOur findings uncover essential roles of the TRIM24-Sox2 axis in GBM stemness and invasiveness, suggesting TRIM24 as a potential target for effective GBM management.

Indexed as

Brain NeoplasmsGlioblastomaCarrier ProteinsCell DifferentiationCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticHumansNeoplastic Stem CellsSOXB1 Transcription FactorsCarrier ProteinsSOX2 protein, humanSOXB1 Transcription FactorsTRIM24 protein, humanglioblastomainvasionSox2stemnessTRIM24

Identifiers

PMID32492707
PMCPMC7746937
OpenAlexW3029608281

What OpenQuestion holds

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Registered trials

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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.