Evidence map›Paper›PMID 42157931›Full record

ArticleInternational journal of biological sciences2026

PRDM16 Drives Thyroid Cancer Differentiation via a TRIM58-MVP Axis to Suppress MAPK and PI3K/AKT Signaling.

Jialong Yu, Wei Luo, Zijie Niu, Miao Zhang, Yunqi Gao, Mengran Tian, Zhongyu Wang, Xing Wan, Han Gui, Qian Su and 6 more

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Article in International journal of biological sciences, 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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1 · What the graph read from it

What it found

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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

16 authors.

Jialong YuDepartment of Thyroid and Neck Tumor, Tianjin Medical University Cancer Institute and Hospital, Tianjin's Clinical Research Center for Cancer, Tianjin, China.
Wei LuoDepartment of Thyroid and Neck Tumor, Tianjin Medical University Cancer Institute and Hospital, Tianjin's Clinical Research Center for Cancer, Tianjin, China.
Zijie NiuDepartment of Thyroid and Neck Tumor, Tianjin Medical University Cancer Institute and Hospital, Tianjin's Clinical Research Center for Cancer, Tianjin, China.
Miao ZhangDepartment of Thyroid and Neck Tumor, Tianjin Medical University Cancer Institute and Hospital, Tianjin's Clinical Research Center for Cancer, Tianjin, China.
Yunqi GaoSchool of Medicine, Nankai University, Tianjin, China.
Mengran TianSchool of Medicine, Nankai University, Tianjin, China.
Zhongyu WangDepartment of Thyroid and Neck Tumor, Tianjin Medical University Cancer Institute and Hospital, Tianjin's Clinical Research Center for Cancer, Tianjin, China.
Xing WanDepartment of Thyroid and Neck Tumor, Tianjin Medical University Cancer Institute and Hospital, Tianjin's Clinical Research Center for Cancer, Tianjin, China.
Han GuiState Key Laboratory of Advanced Medical Materials and Devices, Tianjin Key Laboratory of Radiation Medicine and Molecular Nuclear Medicine, Key Laboratory of Radiopharmacokinetics for Innovative Drugs, Tianjin Institutes of Health Science, Institute of Radiation Medicine, Chinese Academy of Medical Sciences & Peking Union Medical College, Tianjin, China.
Qian SuDepartment of Molecular Imaging and Nuclear Medicine, Tianjin Medical University Cancer Institute and Hospital, Tianjin's Clinical Research Center for Cancer, Tianjin, China.
Wenhao ChenDepartment of Thyroid and Neck Tumor, Tianjin Medical University Cancer Institute and Hospital, Tianjin's Clinical Research Center for Cancer, Tianjin, China.
Linfei HuDepartment of Thyroid and Neck Tumor, Tianjin Medical University Cancer Institute and Hospital, Tianjin's Clinical Research Center for Cancer, Tianjin, China.
Xiukun HouDepartment of Thyroid and Neck Tumor, Tianjin Medical University Cancer Institute and Hospital, Tianjin's Clinical Research Center for Cancer, Tianjin, China.
Qiman DongDepartment of Thyroid and Neck Tumor, Tianjin Medical University Cancer Institute and Hospital, Tianjin's Clinical Research Center for Cancer, Tianjin, China.
Xianhui RuanDepartment of Thyroid and Neck Tumor, Tianjin Medical University Cancer Institute and Hospital, Tianjin's Clinical Research Center for Cancer, Tianjin, China.
Xiangqian ZhengDepartment of Thyroid and Neck Tumor, Tianjin Medical University Cancer Institute and Hospital, Tianjin's Clinical Research Center for Cancer, Tianjin, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Thyroid cancer frequently undergoes dedifferentiation, progressing into poorly differentiated or anaplastic carcinoma, which is characterized by therapeutic resistance and a poor prognosis. Epigenetic dysregulation, particularly histone methylation, plays a critical role in this process. In this study, we identify PRDM16 as an essential regulator of thyroid cancer differentiation. Mechanistically, we demonstrate that PRDM16 catalyzes H3K9 monomethylation at the TRIM58 promoter region, thereby enhancing TRIM58 transcription. Upregulated TRIM58 subsequently promotes ubiquitination and degradation of MVP, leading to suppression of both the MAPK and PI3K/AKT signaling pathways and maintenance of cellular differentiation. This PRDM16-TRIM58-MVP axis modulates proliferation, epithelial-mesenchymal transition, and radioiodine uptake in thyroid cancer cells. Moreover, PRDM16 overexpression enhances the efficacy of MAPK inhibitor-induced redifferentiation therapy. Collectively, these findings establish PRDM16 as a novel tumor suppressor and potential therapeutic target, offering a promising redifferentiation-based strategy for the treatment of advanced thyroid cancer.

Indexed as

Histone MethyltransferasesMajor Vault ProteinMAP Kinase Signaling SystemThyroid Carcinoma, AnaplasticThyroid NeoplasmsAnimalsCell Line, TumorCell Transformation, NeoplasticDNA-Binding ProteinsFemaleHumansMiceMice, Inbred BALB CMice, NudePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktDNA-Binding ProteinsHistone MethyltransferasesMajor Vault ProteinMVP protein, humanPhosphatidylinositol 3-KinasesPRDM16 protein, humanProto-Oncogene Proteins c-aktTranscription FactorsTRIM58 protein, humanTripartite Motif ProteinsdifferentiationMVPPRDM16thyroid cancerTRIM58

Identifiers

PMID42157931
PMCPMC13182561

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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.