Liang Zhang , Fei Li , Lingxue Zhang , Yuyan Zhou , Yusheng Liu , Jing Liu , Yilun Cheng , Jianjun Shu , Haikang Zhao , Yao Wei
{"title":"KIF18B drives the malignant progression of gliomas by activating the Notch pathway","authors":"Liang Zhang , Fei Li , Lingxue Zhang , Yuyan Zhou , Yusheng Liu , Jing Liu , Yilun Cheng , Jianjun Shu , Haikang Zhao , Yao Wei","doi":"10.1016/j.cellsig.2025.111888","DOIUrl":null,"url":null,"abstract":"<div><div>Kinesin family member 18B (KIF18B) is expressed differently in multiple malignancies and contributes to tumorigenesis. However, the relevance of KIF18B in glioma remains undetermined. This work evaluated the level and clinical significance of KIF18B in glioma. The upregulation of KIF18B was frequently detected in glioma specimens, which was related to clinicopathological features and therapeutic outcomes. A decrease in KIF18B expression in glioma cells was found to suppress malignant proliferation and metastasis, while simultaneously enhancing the cells' sensitivity to chemotherapeutic agents. Bioinformatics analysis demonstrated a significant correlation between KIF18B and the Notch signaling pathway in glioma cells. Further experimental validation confirmed that silencing KIF18B effectively inhibited the activation of the Notch signaling pathway. Reactivation of the Notch signaling pathway remarkably reversed the cancer-suppressing effects of KIF18B knockdown. Moreover, the ability of KIF18B-silenced glioma cells to form xenografts in nude mice was markedly impaired, accompanied by the downregulation of the Notch signaling pathway. This work indicates that KIF18 is crucial for maintaining glioma progression and proposes its potential as a promising therapeutic target for glioma treatment.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"134 ","pages":"Article 111888"},"PeriodicalIF":4.4000,"publicationDate":"2025-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cellular signalling","FirstCategoryId":"99","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0898656825003031","RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"CELL BIOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Kinesin family member 18B (KIF18B) is expressed differently in multiple malignancies and contributes to tumorigenesis. However, the relevance of KIF18B in glioma remains undetermined. This work evaluated the level and clinical significance of KIF18B in glioma. The upregulation of KIF18B was frequently detected in glioma specimens, which was related to clinicopathological features and therapeutic outcomes. A decrease in KIF18B expression in glioma cells was found to suppress malignant proliferation and metastasis, while simultaneously enhancing the cells' sensitivity to chemotherapeutic agents. Bioinformatics analysis demonstrated a significant correlation between KIF18B and the Notch signaling pathway in glioma cells. Further experimental validation confirmed that silencing KIF18B effectively inhibited the activation of the Notch signaling pathway. Reactivation of the Notch signaling pathway remarkably reversed the cancer-suppressing effects of KIF18B knockdown. Moreover, the ability of KIF18B-silenced glioma cells to form xenografts in nude mice was markedly impaired, accompanied by the downregulation of the Notch signaling pathway. This work indicates that KIF18 is crucial for maintaining glioma progression and proposes its potential as a promising therapeutic target for glioma treatment.
期刊介绍:
Cellular Signalling publishes original research describing fundamental and clinical findings on the mechanisms, actions and structural components of cellular signalling systems in vitro and in vivo.
Cellular Signalling aims at full length research papers defining signalling systems ranging from microorganisms to cells, tissues and higher organisms.