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Updated: Sep 20, 2025

Isolation and Flow Cytometric Analysis of Glioma-infiltrating Peripheral Blood Mononuclear Cells
Published on: November 28, 2015
KIF18B drives the malignant progression of gliomas by activating the Notch pathway
Liang Zhang1, Fei Li2, Lingxue Zhang2
1Northwest University, No. 1 Xuefu Street, Guodu Education and Technology Industrial Zone, Chang'an District, Xi'an 710127, China; Xi'an Daxing Hospital, No. 353 Laodong North Road, Lianhu District, Xi'an 710016, China; Department of Neurosurgery, Second Affiliated Hospital of Xi'an Medical University, No. 167 Fangdong Street, Xi'an 710038, China.
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.
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