Evidence map›Paper›PMID 41703542›Full record

ArticleMolecular cancer2026

CBFA2T2: a novel H3K27 reader regulating metabolism and tumor growth.

Shengfei He, Yutian Ou, Fangfang Jiao, Jiuxing Feng, Ping Zhu, Jie Ma, Ning Xu, Haitao Li, Rui Guo

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular cancer, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

What it found

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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

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3 · Its place in the literature

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0 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

9 authors.

Shengfei He *Center for Medical Research and Innovation, Shanghai Pudong Hospital, Fudan University Pudong Medical Center, and the Shanghai Key Laboratory of Medical Epigenetics, the International Co-laboratory of Medical Epigenetics and Metabolism, Ministry of Science and Technology, Institutes of Biomedical Sciences, Fudan University, Shanghai, 200032, China.
Yutian Ou *State Key Laboratory of Molecular Oncology, MOE Key Laboratory of Protein Sciences, Beijing Frontier Research Center for Biological Structure, School of Basic Medical Sciences, Tsinghua Medicine, Tsinghua University, Beijing, 100084, China.
Fangfang JiaoState Key Laboratory of Eye Health, Department of Ophthalmology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200011, China.
Jiuxing FengInstitutes of Biomedical Sciences, Fudan University, Shanghai, 200032, China.
Ping ZhuGuangdong Cardiovascular Institute, Guangdong Provincial People's Hospital(Guangdong Academy of Medical Sciences),Southern Medical University, Guangzhou, Guangdong, 510100, China.
Jie MaDepartment of Pediatric Neurosurgery, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200092, China.
Ning XuState Key Laboratory of Molecular Oncology, MOE Key Laboratory of Protein Sciences, Beijing Frontier Research Center for Biological Structure, School of Basic Medical Sciences, Tsinghua Medicine, Tsinghua University, Beijing, 100084, China.
Haitao LiState Key Laboratory of Molecular Oncology, MOE Key Laboratory of Protein Sciences, Beijing Frontier Research Center for Biological Structure, School of Basic Medical Sciences, Tsinghua Medicine, Tsinghua University, Beijing, 100084, China. lht@tsinghua.edu.cn.
Rui GuoCenter for Medical Research and Innovation, Shanghai Pudong Hospital, Fudan University Pudong Medical Center, and the Shanghai Key Laboratory of Medical Epigenetics, the International Co-laboratory of Medical Epigenetics and Metabolism, Ministry of Science and Technology, Institutes of Biomedical Sciences, Fudan University, Shanghai, 200032, China. guorui@fudan.edu.cn.

Funding

Ministry of Science and Technology of the People's Republic of China 2018YFA0108700Ministry of Science and Technology of the People's Republic of China 2021YFA1300100; 2020YFA0803303National Natural Science Foundation of China 31571318, 31771450, 32170584National Natural Science Foundation of China 92153302 and 32230019
6 · The paper itself

Abstract

Histone H3.3K27M mutations are identified in diffuse midline glioma (DMG), resulting in a global reduction in H3K27me3. Analyzing the histone recognition mechanism at H3K27 position can enhance the understanding of this highly lethal mutation. Here we identify a novel histone reader CBFA2T2, which recognizes non-mutated or un-modified histone H3K27. Biochemical assays confirm this binding specificity, indicating that it is mediated by NHR2 domain of CBFA2T2. CBFA2T2 represses the transcription of metabolic genes involved in carbon metabolism, glycolysis/gluconeogenesis and the TCA cycle pathways through its binding to H3K27, thereby regulating metabolite levels. These alter the alpha-ketoglutarate/Succinate ratio and indirectly impacts H3K27me3 level, through affecting the H3K27me3 demethylases. Our results uncover a novel mechanism by which CBFA2T2 transcriptionally regulates metabolism and tumor growth in H3.3K27M cells. These findings suggest that CBFA2T2 and its targeted genes may serve as potential therapeutic targets for the treatment of H3.3K27M cancer.

Indexed as

GliomaHistonesAnimalsCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticHumansMutationProtein BindingHistonesCBFA2T2H3.3K27MH3K27 readerMetabolism

Identifiers

PMID41703542
PMCPMC13081504

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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.