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Research Article

KDM6B: A critical epigenetic regulator in glioma pathogenesis and therapeutic targeting

Aixia Sui
1*
Xiaoqiang Guo
2*

1 Department of Oncology, Hebei General Hospital, Shijiazhuang, Hebei

2 Department of Kinesiology, Hebei Sport University, Shijiazhuang, Hebei



Tumor Discovery 2026, 5(3),025520132; https://doi.org/10.36922/TD025520132
Submitted26 Dec 2025
Revised26 Feb 2026
Accepted02 Mar 2026
Published05 May 2026
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Cite This Article
Aixia Sui ,Xiaoqiang Guo . (2026). <p>KDM6B: A critical epigenetic regulator in glioma pathogenesis and therapeutic targeting</p>. Tumor Discovery , 5(3), TD025520132. https://doi.org/10.36922/TD025520132
Abstract

Gliomas are among the most aggressive malignant brain tumors, and the clinical efficacy of current treatment modalities (e.g., surgical resection, radiotherapy, and chemotherapy) is far from satisfactory, resulting in dismal prognostic outcomes for patients. In recent years, aberrant histone modification has been identified as a crucial driver of glioma initiation and progression, opening up a novel and promising research direction for exploring the molecular mechanisms of gliomagenesis and developing targeted therapeutic strategies. Histone lysine demethylase 6B (KDM6B), also known as JmjC-containing protein D3 (JMJD3), exerts its biological function by catalyzing the demethylation of the repressive histone mark H3K27me2/3, thereby activating downstream gene transcription and participating in numerous physiological and pathological processes, such as neurogenesis, cell differentiation, and immune regulation. Abnormal expression or dysregulated enzymatic activity of KDM6B can disrupt multiple key signaling pathways associated with glioma development, leading to uncontrolled cell proliferation, enhanced invasion and infiltrative growth, and resistance to therapies. KDM6B represents a potential biomarker for the tumor grading and prognostic evaluation of glioma, with its clinical diagnostic value awaiting further large-scale clinical validation. Moreover, in vitro cell experiments and in vivo animal models have shown that targeted inhibition of KDM6B can effectively inhibit glioma progression. These advances have deepened our understanding of the epigenetic regulatory mechanisms underlying glioma development and hold great promise for improving the clinical therapeutic efficacy of glioma treatments.

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