Evidence map›Paper›PMID 40604866›Full record

ArticleEuropean journal of medical research2025

Pleiotrophin promote glioma proliferation and invasion by enhancing NF-κB/SLUG mediated epithelial-mesenchymal transition.

Hong-Xing Ye, Chao Zhang, Long-Yuan He, Ping Lan, Feng Wang, Ren-Ya Zhan, Xiu-Jue Zheng

Abstract read
In one paragraph

Article in European journal of medical research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
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.

Hong-Xing YeDepartment of Neurosurgery, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
Chao ZhangDepartment of Neurosurgery, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
Long-Yuan HeZhejiang University School of Medicine, Hangzhou, Zhejiang, China.
Ping LanDepartment of Neurosurgery, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
Feng WangDepartment of Neurosurgery, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
Ren-Ya ZhanDepartment of Neurosurgery, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
Xiu-Jue ZhengDepartment of Neurosurgery, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China. zxj8065@zju.edu.cn.

Funding

the Zhejiang Provincial Natural Science Foundation of China LY18H160020
6 · The paper itself

Abstract

backgroundGliomas are aggressive brain tumors with high mortality and recurrence rates. Pleiotrophin (PTN), a cytokine that interacts with heparin, is upregulated in several cancers, including breast and lung cancer. PTN is implicated in cancer progression, recurrence, epithelial-mesenchymal transition (EMT), and metastasis. However, the role of PTN in glioma progression remains poorly understood. This study aimed to investigate the expression profile of PTN in glioma and its potential prognostic significance.

methodsThe expression levels of PTN in glioma samples were analyzed using data from The Cancer Genome Atlas (TCGA) and the Chinese Glioma Genome Atlas (CGGA). Gene Ontology (GO) term analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis were conducted to identify PTN-associated pathways. In vitro experiments were performed to assess the impact of PTN suppression on glioma cell growth, cell cycle progression, migration, and invasion. In addition, gene set enrichment analysis (GSEA) and Western blot were employed to investigate the link between PTN and NF-κB signaling pathways.

resultsPTN expression was significantly higher in glioma samples, and elevated PTN levels were associated with decreased overall survival. GO term and KEGG analysis showed that PTN is primarily linked to pathways related to cell mitosis, including the cell cycle and DNA replication. In vitro experiments demonstrated that the suppression of PTN inhibited glioma cell growth, arrested the cell cycle in the G0/G1 phase, and impaired the migratory and invasive capabilities of glioma cells. GSEA revealed a significant correlation between PTN and the NF-κB pathway. Further investigation showed that PTN suppression inhibited NF-κB activation and IκB phosphorylation, thereby preventing Slug-induced EMT in glioma cells.

conclusionsPTN plays a crucial role in glioma progression by regulating cell proliferation, migration, invasion, and EMT through the NF-κB pathway. PTN may serve as an important prognostic biomarker and therapeutic target in glioma treatment.

Indexed as

Brain NeoplasmsCarrier ProteinsCytokinesEpithelial-Mesenchymal TransitionGliomaNF-kappa BCell Line, TumorCell MovementCell ProliferationGene Expression Regulation, NeoplasticHumansNeoplasm InvasivenessPrognosisSignal TransductionCarrier ProteinsCytokinesNF-kappa BpleiotrophinEpithelial–mesenchymal transitionGliomaNF-κB pathwayPleiotrophinProliferation and invasion

Identifiers

PMID40604866
PMCPMC12220309

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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.