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REVIEW ARTICLE

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

Aixia Sui1* ,  Xiaoqiang Guo2*
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1 Department of Oncology, Hebei General Hospital, Shijiazhuang, Hebei, China
2 Department of Kinesiology, Hebei Sport University, Shijiazhuang, Hebei, China
Tumor Discovery, 025520132 https://doi.org/10.36922/TD025520132
Received: 26 December 2025 | Revised: 26 February 2026 | Accepted: 2 March 2026 | Published online: 5 May 2026
© 2026 by the Author(s). This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution 4.0 International License ( https://creativecommons.org/licenses/by/4.0/ )
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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.

Keywords
Glioma
Histone demethylase
KDM6B
H3K27me2/3
Epigenetic regulation
Targeted therapy
Funding
None.
Conflict of interest
The authors declare they have no competing interests.
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