Evidence map›Paper›PMID 41291235›Full record

ArticleCellular and molecular life sciences : CMLS2025

Histone demethylase KDM9 activates the CCND1/AKT pathway to promote the malignant progression of gliomas through interaction with BRD2.

Jin Cheng, Xingzhi Peng, Siyuan Tang, Peijun Zhou, Zhuan Zhou, Zenghui Mao, Dan Li, Lifang Yang, Jinwu Peng

Abstract read
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In one paragraph

Article in Cellular and molecular life sciences : CMLS, 2025. 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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1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

9 authors.

Jin Cheng *Department of Oncology, Key Laboratory of Carcinogenesis and Cancer Invasion of Ministry of Education, National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, 410078, China.
Xingzhi Peng *Department of Oncology, Key Laboratory of Carcinogenesis and Cancer Invasion of Ministry of Education, National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, 410078, China.
Siyuan TangDepartment of Oncology, Key Laboratory of Carcinogenesis and Cancer Invasion of Ministry of Education, National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, 410078, China.
Peijun ZhouDepartment of Oncology, Key Laboratory of Carcinogenesis and Cancer Invasion of Ministry of Education, National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, 410078, China.
Zhuan ZhouCancer Research Institute, Xiangya School of Basic Medicine Science, Central South University, Changsha, 410078, China.
Zenghui MaoHunan Provincial Key Laboratory of Regional Hereditary Birth Defects Prevention and Control, Changsha Hospital for Maternal & Child Health Care Affiliated to Hunan Normal University, Changsha, 410007, China.
Dan LiDepartment of Life Science, College of Biology, Hunan University, Changsha, 410012, China.
Lifang YangDepartment of Oncology, Key Laboratory of Carcinogenesis and Cancer Invasion of Ministry of Education, National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, 410078, China. yanglifang@csu.edu.cn.ORCID http://orcid.org/0000-0002-3012-8350
Jinwu PengDepartment of Pathology, Xiangya Hospital, Central South University, Changsha, 410078, China. jinwupeng@csu.edu.cn.

Funding

National Natural Science Foundation of China 82372683Natural Science Foundation of Hunan Province 2022JJ30059Natural Science Foundation of Hunan Province 2023JJ40067Natural Science Foundation of Hunan Province 2025JJ60588
6 · The paper itself

Abstract

Gliomas are highly aggressive brain tumors with limited treatment options, thus, it is necessary to identify new molecular targets for therapeutic intervention. Epigenetic aberration plays a vital role in the malignant progression of tumors. KDM9 is a histone demethylase, but its function and mechanism in tumors remain unclear. In the present study, we found that KDM9 was highly expressed in malignant gliomas and that it promoted the proliferation, invasion, stem-like characteristics, and temozolomide (TMZ) resistance of tumor cells. Mechanistically, KDM9 mediated the demethylation of H4K20me2 on the CCND1 promoter and interacted with the transcription factor BRD2 to facilitate CCND1 transcription, further enhancing the AKT signaling pathway, thereby promoting the malignant progression and TMZ resistance of glioma cells. In vivo experiments also demonstrated that KDM9 knockdown suppressed xenograft growth and TMZ resistance. Our study clarified the role and mechanism of the epigenetic regulatory molecule KDM9 in the malignant progression and drug resistance of gliomas, thus providing a potential predictive and interventional target for glioma.

Indexed as

Brain NeoplasmsCyclin D1GliomaHistone DemethylasesProtein Serine-Threonine KinasesProto-Oncogene Proteins c-aktAnimalsBromodomain Containing ProteinsCell Line, TumorCell ProliferationDisease ProgressionDrug Resistance, NeoplasmGene Expression Regulation, NeoplasticHumansMiceMice, NudeBRD2 protein, humanBromodomain Containing ProteinsCCND1 protein, humanCyclin D1Histone DemethylasesProtein Serine-Threonine KinasesProto-Oncogene Proteins c-aktTemozolomideTranscription FactorsBRD2CCND1GliomaKDM9TMZ sensitivity

Identifiers

PMID41291235
PMCPMC12647419

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LicenceCC BY-NC-ND
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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.