Evidence map›Paper›PMID 40971867›Full record

ArticleNeuro-oncology2026

EGFR/ZBED1 reciprocal regulation promotes stemness and tumorigenesis in glioblastoma.

Nana Hou, Yutao Wang, Qiuxiang You, Lei Zhang, Wenjia Zhang, Xinyi Wang, Chunyan Deng, Jiachuan Yan, Saiyu Cheng, Jianwen Ji and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neuro-oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

13 authors.

Nana HouDepartment of Neurology and Neurosurgery, the Third Affiliated Hospital of Chongqing Medical University, Chongqing, China (N.H., Y.W., Q.Y., L.Z., W.Z., X.W., C.D., J.Y., S.C., J.J., Y.Z.).
Yutao WangDepartment of Neurology and Neurosurgery, the Third Affiliated Hospital of Chongqing Medical University, Chongqing, China (N.H., Y.W., Q.Y., L.Z., W.Z., X.W., C.D., J.Y., S.C., J.J., Y.Z.).
Qiuxiang YouDepartment of Neurology and Neurosurgery, the Third Affiliated Hospital of Chongqing Medical University, Chongqing, China (N.H., Y.W., Q.Y., L.Z., W.Z., X.W., C.D., J.Y., S.C., J.J., Y.Z.).
Lei ZhangDepartment of Neurology and Neurosurgery, the Third Affiliated Hospital of Chongqing Medical University, Chongqing, China (N.H., Y.W., Q.Y., L.Z., W.Z., X.W., C.D., J.Y., S.C., J.J., Y.Z.).
Wenjia ZhangDepartment of Neurology and Neurosurgery, the Third Affiliated Hospital of Chongqing Medical University, Chongqing, China (N.H., Y.W., Q.Y., L.Z., W.Z., X.W., C.D., J.Y., S.C., J.J., Y.Z.).
Xinyi WangDepartment of Neurology and Neurosurgery, the Third Affiliated Hospital of Chongqing Medical University, Chongqing, China (N.H., Y.W., Q.Y., L.Z., W.Z., X.W., C.D., J.Y., S.C., J.J., Y.Z.).
Chunyan DengDepartment of Neurology and Neurosurgery, the Third Affiliated Hospital of Chongqing Medical University, Chongqing, China (N.H., Y.W., Q.Y., L.Z., W.Z., X.W., C.D., J.Y., S.C., J.J., Y.Z.).
Jiachuan YanDepartment of Neurology and Neurosurgery, the Third Affiliated Hospital of Chongqing Medical University, Chongqing, China (N.H., Y.W., Q.Y., L.Z., W.Z., X.W., C.D., J.Y., S.C., J.J., Y.Z.).
Saiyu ChengDepartment of Neurology and Neurosurgery, the Third Affiliated Hospital of Chongqing Medical University, Chongqing, China (N.H., Y.W., Q.Y., L.Z., W.Z., X.W., C.D., J.Y., S.C., J.J., Y.Z.).
Jianwen JiDepartment of Neurology and Neurosurgery, the Third Affiliated Hospital of Chongqing Medical University, Chongqing, China (N.H., Y.W., Q.Y., L.Z., W.Z., X.W., C.D., J.Y., S.C., J.J., Y.Z.).
Jianbing HouJinfeng Laboratory, Chongqing, China (J.H., H.C.).
Hongjuan CuiJinfeng Laboratory, Chongqing, China (J.H., H.C.).
Yundong ZhangDepartment of Neurology and Neurosurgery, the Third Affiliated Hospital of Chongqing Medical University, Chongqing, China (N.H., Y.W., Q.Y., L.Z., W.Z., X.W., C.D., J.Y., S.C., J.J., Y.Z.).

Funding

National Natural Science Foundation of China 82473181Natural Science Foundation of Chongqing CSTB2024NSCQ-LZX0096Science and Technology Major Project of Guangxi AA24011002
6 · The paper itself

Abstract

backgroundGlioblastoma stem cells (GSCs), a stem-like tumorigenic subpopulation within glioblastoma (GBM), exhibit remarkable self-renewal capacity and therapeutic resistance. Zinc finger BED domain-containing protein 1 (ZBED1), a dual-function transcription factor and SUMO E3 ligase, has been implicated in oncogenic processes across malignancies, its functional role and regulatory mechanisms in GSCs remain enigmatic.

methodsMultimodal approaches including, immunohistochemistry, immunoblotting, and immunofluorescence, were employed to evaluate ZBED1 expression patterns in GSCs and clinical GBM specimens. Functional characterization utilized in vitro models (proliferation assays, tumor-sphere formation assays, and limiting dilution analysis) complemented by in vivo orthotopic xenograft models. Mechanistic investigations integrated RNA sequencing, label-free proteomics, chromatin immunoprecipitation (ChIP), immunohistochemistry, and western blotting to delineate the EGFR/ZBED1 regulatory axis.

resultsWe demonstrated that ZBED1 was significantly upregulated in GSCs and linked to unfavorable prognosis. Genetic ablation of ZBED1 significantly impaired GSC proliferation and self-renewal capacity while extending survival in xenograft models. Mechanistically, EGFR-mediated ZBED1 phosphorylation at tyrosine residues Y160/Y513 enhanced ZBED1-UBC9 interaction, promoting SUMOylation-dependent protein stabilization. Remarkably, ZBED1 reciprocally sustained EGFR expression through transcriptional repression of the E3 ubiquitin ligase PARK2, establishing a self-reinforcing EGFR/ZBED1/PARK2 signaling circuit critical for GSC maintenance.

conclusionsOur findings elucidate a novel EGFR/ZBED1 positive feedback loop that drives GSC propagation and tumorigenesis, highlighting ZBED1 as an attractive candidate for therapeutic targeting in GBM.

Indexed as

Brain NeoplasmsCarcinogenesisGene Expression Regulation, NeoplasticGlioblastomaNeoplastic Stem CellsRepressor ProteinsTranscription FactorsAnimalsCell ProliferationErbB ReceptorsHumansMiceMice, NudePrognosisTumor Cells, CulturedEGFR protein, humanErbB ReceptorsRepressor ProteinsTranscription FactorsEGFRglioblastoma | phosphorylationSUMOylationZBED1

Identifiers

PMID40971867
PMCPMC12979038

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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.