Evidence map›Paper›PMID 36575317›Full record

ArticleCancer gene therapy2023

Transcription factor YY1 mediates self-renewal of glioblastoma stem cells through regulation of the SENP1/METTL3/MYC axis.

Jian You, Bei Tao, Lilei Peng, Tangming Peng, Haiping He, Shan Zeng, Jizhong Han, Ligang Chen, Xiangguo Xia, Xiaobo Yang and 1 more

Abstract read
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In one paragraph

Article in Cancer gene therapy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

19 citing papers in PubMed, 27 citations in OpenAlex.

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  7. Yin Yang 1: Function, Mechanisms, and Glia.Neurochemical research · 2025
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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

11 authors at 2 institutions in 1 country.

Jian YouDepartment of Neurosurgery, The Affiliated Hospital of Southwest Medical University, 646000, Luzhou, P. R. China.
Bei TaoRheumatism Department, The Affiliated Hospital of Southwest Medical University, 646000, Luzhou, P. R. China.
Lilei PengDepartment of Neurosurgery, The Affiliated Hospital of Southwest Medical University, 646000, Luzhou, P. R. China.
Tangming PengDepartment of Neurosurgery, The Affiliated Hospital of Southwest Medical University, 646000, Luzhou, P. R. China.
Haiping HeDepartment of Neurosurgery, The Affiliated Hospital of Southwest Medical University, 646000, Luzhou, P. R. China.
Shan ZengDepartment of Neurosurgery, The Affiliated Hospital of Southwest Medical University, 646000, Luzhou, P. R. China.
Jizhong HanDepartment of Neurosurgery, The Affiliated Hospital of Southwest Medical University, 646000, Luzhou, P. R. China.
Ligang ChenDepartment of Neurosurgery, The Affiliated Hospital of Southwest Medical University, 646000, Luzhou, P. R. China.
Xiangguo XiaDepartment of Neurosurgery, The Affiliated Hospital of Southwest Medical University, 646000, Luzhou, P. R. China.
Xiaobo YangDepartment of Neurosurgery, The Affiliated Hospital of Southwest Medical University, 646000, Luzhou, P. R. China. xbyang710@swmu.edu.cn.ORCID 0000-0002-6151-9784
Chuanhong ZhongDepartment of Neurosurgery, The Affiliated Hospital of Southwest Medical University, 646000, Luzhou, P. R. China. zhongchuanhong@swmu.edu.cn.ORCID 0000-0002-1436-4062
Affiliated Hospital of Southwest Medical University · CNSouthwest Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioma is a primary brain tumor with limited treatment approaches and glioblastoma stem cells (GSCs) are manifested with the self-renewal capability and high tumorigenic capacity. This study was performed to investigate the regulatory effect of the SUMO-specific protease 1 (SENP1)/methyltransferase-like 3 (METTL3)/MYC axis on the self-renewal of GSCs mediated by transcription factor Yin Yang 1 (YY1). Following bioinformatics analysis and clinical and cellular experiments, we found that YY1 was highly expressed in GBM tissues and cells, while silencing its expression reduced the self-renewal ability of GSCs. Functionally, YY1 promoted the transcriptional expression of SENP1 by binding to the promoter region of SENP1, while the deSUMOase SENP1 facilitated the methylase activity of m6A through deSUMOylation of the methylase METTL3, thereby promoting the m6A modification of MYC mRNA via METL3 and promoting the expression of MYC. A nude mouse xenograft model of GBM was also constructed to examine the tumorigenicity of GSCs. The obtained findings demonstrated that YY1 promoted tumorigenicity of GSCs by promoting the expression of MYC in vivo. Conclusively, YY1 can transcriptionally upregulate the SUMOylase SENP1 and enhance the methylase activity of METTL3, resulting in the increased m6A modification level of MYC mRNA, thereby promoting the self-renewal of GSCs.

Indexed as

Brain NeoplasmsGlioblastomaAnimalsCell Line, TumorCell ProliferationCysteine EndopeptidasesHumansMethyltransferasesMiceNeoplastic Stem CellsPeptide HydrolasesRNA, MessengerYY1 Transcription FactorCysteine EndopeptidasesMethyltransferasesMETTL3 protein, humanMettl3 protein, mousePeptide HydrolasesRNA, MessengerSENP1 protein, humanSenp1 protein, mouseYY1 protein, humanYY1 Transcription Factor

Identifiers

PMID36575317
OpenAlexW4313236456

What OpenQuestion holds

Textmetadata
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.