ELF3 drives glioblastoma multiforme progression through the regulation of MXRA8 expression.
Overview
- Department of Neurosurgery, Changhai Hospital of the Naval Medical University,Shanghai, 200434 China
- Department of Pathology, Naval Medical Center of PLA, No. 338 Huaihai West Road, Shanghai, 200052 China
- Department of Neurosurgery, Bozhou District People’s Hospital of Zunyi City,Zunyi City, Guizhou Province 563100 China
Abstract
The abstract is not reproduced here: the paper's license (CC BY-NC-ND) does not allow it. Read it in the paper, at the publisher or on Europe PMC.
Code
The paper links to its data, not to its authors' code: see the Data section.
Tracing map
A tracing map links a paper to the code its authors published: this paper has none, so it has no map.
Data
Datasets cited
- doi:10.7910/
dvn/ , at the source; found in “Data availability”ufhs7z](https:/ doi.org/ 10.7910/ dvn/ ufhs7z)
Data availability statement
The paper has a data availability statement. Its license (CC BY-NC-ND) does not allow reproducing it here; in short, from what the harvester recognized in it:
- it points to a dataset: DOI 10.7910/
dvn/ ufhs7z](https:/ doi.org/ 10.7910/ dvn/ ufhs7z)
Read it in the paper: doi.org/10.1038/s41598-026-46657-w.
Versions
The history of this record: each version stored by the harvester or made by a correction of its authors or of the maintainers of its code, and what changed in its facts. The texts of the paper (its abstract, its availability statements) are not part of it; versions that changed only those are not listed.
Version 1, 28 September 2026: the first record
Recorded: type, language, journal, volume, issue, pages, dates, 6 authors, 9 keywords, 16 MeSH terms, 1 funder, 22 references.
Cite
This paper
Wang, M., Bo, H., Chen, D., Mao, J., Miao, Z., & Wang, L. (2026). ELF3 drives glioblastoma multiforme progression through the regulation of MXRA8 expression. Scientific reports, 16(1), 15380. https://
BibTeX
@article{wang2026elf3,
author = {Wang, Maomao and Bo, Haiji and Chen, Dapeng and Mao, Jiangxin and Miao, Zong and Wang, Laixing},
title = {{ELF3 drives glioblastoma multiforme progression through the regulation of MXRA8 expression}},
journal = {Scientific reports},
year = {2026},
month = apr,
volume = {16},
number = {1},
pages = {15380},
publisher = {Nature Publishing Group},
issn = {2045-2322},
doi = {10.1038/
url = {https://
pmid = {41922512},
pmcid = {PMC13183993}
}
RIS
TY - JOUR
AU - Wang, Maomao
AU - Bo, Haiji
AU - Chen, Dapeng
AU - Mao, Jiangxin
AU - Miao, Zong
AU - Wang, Laixing
TI - ELF3 drives glioblastoma multiforme progression through the regulation of MXRA8 expression
T2 - Scientific reports
J2 - Sci Rep
PY - 2026
DA - 2026/
VL - 16
IS - 1
SP - 15380
SN - 2045-2322
PB - Nature Publishing Group
DO - 10.1038/
UR - https://
LA - en
ER -
CSL-JSON
{
"id": "10.1038/
"type": "article-journal",
"title": "ELF3 drives glioblastoma multiforme progression through the regulation of MXRA8 expression",
"container-title": "Scientific reports",
"author": [
{
"family": "Wang",
"given": "Maomao"
},
{
"family": "Bo",
"given": "Haiji"
},
{
"family": "Chen",
"given": "Dapeng"
},
{
"family": "Mao",
"given": "Jiangxin"
},
{
"family": "Miao",
"given": "Zong"
},
{
"family": "Wang",
"given": "Laixing"
}
],
"container-title-short":
"volume": "16",
"issue": "1",
"page": "15380",
"DOI": "10.1038/
"PMID": "41922512",
"PMCID": "PMC13183993",
"ISSN": "2045-2322",
"publisher": "Nature Publishing Group",
"URL": "https://
"language": "en",
"issued": {
"date-parts": [
[
2026,
4,
1
]
]
}
}
Similar papers
The papers with a page that share the most with this one: the tools found in their code, their categories, datasets, cited references and authors, the rarest counting most.
- [1] doi:10.1038/s41467-026-73852-0
- LRP4 is an entry receptor for multiple encephalitic alphaviruses.Journal: Nature communicationsIn common: other condition, mouse, cellular / molecular, 1 reference
- [2] doi:10.1038/s42003-026-09915-1
- Single cell and spatial sequencing analysis of cancer associated fibroblasts in the brain metastasis tumor microenvironment.Journal: Communications biologyIn common: other condition, cellular / molecular, 1 reference
- [3] doi:10.1186/s12967-026-08266-z [code]
- Single-cell multi-omic integration analysis prioritizes druggable genes and reveals cell-type-specific causal effects in glioblastomagenesis.Journal: Journal of translational medicineIn common: other condition, cellular / molecular, 1 reference
- [4] doi:10.1007/s00262-026-04390-3 [code]
- Identification and prioritisation of tumour antigen candidates from 79 glioblastoma transcriptomes.Journal: Cancer immunology, immunotherapy : CIIIn common: other condition, cellular / molecular, 1 reference
- [5] doi:10.1371/journal.pone.0349101
- Overexpression of key complement regulators in glioblastoma.Journal: PloS oneIn common: other condition, cellular / molecular, 1 reference
- [6] doi:10.3389/fonc.2026.1927290
- Arylsulfatase D promotes malignant phenotypes in glioblastoma cells and is linked to altered Hippo pathway phosphorylation.Journal: Frontiers in oncologyIn common: other condition, cellular / molecular, 1 reference
- [7] doi:10.3390/biology15141179
- Transcriptomic Evidence Identifies Two TMBIM Subgroups with Opposing Prognostic Associations in Glioma.Journal: BiologyIn common: other condition, 1 reference
- [8] doi:10.1002/advs.77551
- Targeting the KAT7/
H3K14ac/ RAC2 Axis Mediates OXPHOS to Promote Stemness Maintenance and Malignancy in Glioblastoma. Journal: Advanced science (Weinheim, Baden-Wurttemberg, Germany)In common: other condition, 1 reference - [9] doi:10.3389/fphar.2026.1797067
- Network-driven prioritization and functional phenotyping nominate TTC23 as a biomarker-informed target in chlorpromazine repurposing for glioblastoma.Journal: Frontiers in pharmacologyIn common: other condition, 1 reference
- [10] doi:10.1007/s12672-026-05166-y [code]
- Single-cell profiling identifies a pro-tumoral VCAN positive macrophage subset and defines a prognostic signature in glioblastoma.Journal: Discover oncologyIn common: other condition, 1 reference
Contribute
The authors of this paper can claim it, correct its record and validate its tracing map, and the maintainers of its code (its owner, or a public member of its organization) correct what it says of their repository; anyone signed in can ask for its removal. Every request goes to OSCR's own machine, which answers it; your account page follows them.
Sign in with ORCID to claim this paper as one of its authors, correct its record or validate its tracing map: when the paper's metadata lists your ORCID iD, you are recognized at once. Maintainers of its code: sign in with GitHub, then claim the repository on your account page.
Claim this paper
Correct its record
Say what each link of this record is, remove the ones that are not the paper's, add the ones that are missing. The correction becomes a new version of the record, in its Versions section.
Request its removal
To ask OSCR to remove this record, the copies of its authors' scripts or its tracing map, use the removal request page: signed in, you say who you are, what to remove and why, then review and confirm the request. Published rules decide every request (how).
Discussion, reproductions, activity
Discussion: questions and error reports about this paper and its code, from signed-in readers and its authors. It opens with sign-in.
Reproductions: reports from readers who ran the authors' code: what they reproduced, with which environment, commit and data. It opens with sign-in.
Activity: what happens around this paper: new versions of its record, its map's validation, discussions and reproductions. It opens with sign-in.