Evidence map›Paper›PMID 41527058›Full record

ArticleBMC cancer2026

MiR-218-5p inhibits glioma progression by targeting CKLF-like MARVEL transmembrane domain-containing 3.

Xiangying Li, Ting Lu, Tong Wang, Jianwei Zhuo, Zhengquan Yu, Gang Cui, Haitao Shen

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in BMC cancer, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Article
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

7 authors.

Xiangying Li *Department of Neurosurgery & Brain and Nerve Research Laboratory, The First Affiliated Hospital of Soochow University, 188 Shizi Street, Suzhou, 215006, China.
Ting Lu *Department of Neurosurgery & Brain and Nerve Research Laboratory, The First Affiliated Hospital of Soochow University, 188 Shizi Street, Suzhou, 215006, China.
Tong WangDepartment of Neurosurgery & Brain and Nerve Research Laboratory, The First Affiliated Hospital of Soochow University, 188 Shizi Street, Suzhou, 215006, China.
Jianwei ZhuoDepartment of Neurosurgery & Brain and Nerve Research Laboratory, The First Affiliated Hospital of Soochow University, 188 Shizi Street, Suzhou, 215006, China.
Zhengquan YuDepartment of Neurosurgery & Brain and Nerve Research Laboratory, The First Affiliated Hospital of Soochow University, 188 Shizi Street, Suzhou, 215006, China.
Gang CuiDepartment of Neurosurgery & Brain and Nerve Research Laboratory, The First Affiliated Hospital of Soochow University, 188 Shizi Street, Suzhou, 215006, China. 2445133252@qq.com.
Haitao ShenDepartment of Neurosurgery & Brain and Nerve Research Laboratory, The First Affiliated Hospital of Soochow University, 188 Shizi Street, Suzhou, 215006, China. dagezi120@126.com.

Funding

Science and Technology Special Fund of Jiangsu Province (Key Research and Development Program for Social Development) BE2023712Suzhou Medical Technology Innovation Project-Clinical Frontier SKY2022002
6 · The paper itself

Abstract

backgroundThis study aimed to investigate the role of miR-218-5p and CKLF-like marvel transmembrane domain-containing 3 (CMTM3) and the interaction between them in glioma.

methodsThe presence of CMTM3 in glioma cells and tissues was detected using immunohistochemical analysis, quantitative reverse transcription polymerase chain reaction, and western blotting. Public databases were used to examine the relationship between CMTM3 expression and patient survival. Transwell assay was performed to evaluate the invasive potential of glioma cells with downregulated CMTM3. Luciferase reporter assay was performed to validate the role of miR-218-5p in regulating CMTM3 expression. Intracranial xenograft models were established to investigate the role of CMTM3 in glioma in vivo.

resultsCMTM3 was upregulated in glioma cells and tissues. Higher CMTM3 expression was significantly associated with shorter overall survival and more advanced clinicopathological characteristics in patients with glioma. Functional assays demonstrated that downregulation of CMTM3 potently suppressed the proliferative and invasive abilities of glioma cells in vitro and reduced tumor growth by approximately 66% in an intracranial xenograft model. Transfection with a miR-218-5p mimic suppressed CMTM3 expression by approximately 68% at the mRNA level and 70% at the protein level in glioma cell lines, indicating that CMTM3 was directly regulated by miR-218-5p. Additionally, the miR-218-5p mimic significantly inhibited the proliferative and invasive abilities of glioma cells.

conclusionMiR-218-5p regulates the oncogenic role of CMTM3 in glioma. Therefore, targeting the miR-218-5p/CMTM3 axis is a promising therapeutic strategy for glioma.

Indexed as

Brain NeoplasmsChemokinesGliomaMARVEL Domain-Containing ProteinsMicroRNAsAnimalsCell Line, TumorCell MovementCell ProliferationDisease ProgressionFemaleGene Expression Regulation, NeoplasticHumansMaleMiceMice, NudeChemokinesCMTM3 protein, humanMARVEL Domain-Containing ProteinsMicroRNAsMIRN218 microRNA, humanCMTM3GliomaMiRNA-218-5pProgression

Identifiers

PMID41527058
PMCPMC12903727

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LicenceCC BY-NC-ND
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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.