ArticleNature communications2017
Targeted inhibition of STAT/TET1 axis as a therapeutic strategy for acute myeloid leukemia.
Erratum issuedOpen access · goldAbstract read
In one paragraph
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 40 papers.
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40citing papers in PubMed
4.5field-weighted citation impact, top 5% of its field
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Who cites it
40 citing papers in PubMed, 66 citations in OpenAlex.
- Electroacupuncture activates the TET1/PPARα pathway to protect mitochondrial function in MASLD.Journal of inflammation (London, England) · 2026Article
- TET1 as a master regulator controlling GPX4-dependent and -independent ferroptosis surveillance in acute myeloid leukemia.Nature communications · 2026Article
- TET knockout cells transit between pluripotent states and exhibit precocious germline entry.The EMBO journal · 2025Article
- TET1: The epigenetic architect of clinical disease progression.Genes & diseases · 2025Review
- Ten-Eleven Translocation Family Proteins: Structure, Biological Functions, Diseases, and Targeted Therapy.MedComm · 2025Review
- Liver TET1 promotes metabolic dysfunction-associated steatotic liver disease.EMBO molecular medicine · 2025Article
- Epigenetics-targeted drugs: current paradigms and future challenges.Signal transduction and targeted therapy · 2024Review
- TET1 Regulates Nestin Expression and Human Airway Smooth Muscle Proliferation.American journal of respiratory cell and molecular biology · 2024Article
- Review
- High STAT4 expression correlates with poor prognosis in acute myeloid leukemia and facilitates disease progression by upregulating VEGFA expression.Open medicine (Warsaw, Poland) · 2024Article
- TET (Ten-eleven translocation) family proteins: structure, biological functions and applications.Signal transduction and targeted therapy · 2023Review
- Hybrids of Sterically Hindered Phenols and Diaryl Ureas: Synthesis, Switch from Antioxidant Activity to ROS Generation and Induction of Apoptosis.International journal of molecular sciences · 2023Article
- Phosphorylation stabilized TET1 acts as an oncoprotein and therapeutic target in B cell acute lymphoblastic leukemia.Science translational medicine · 2023Article
- The prognostic role of C-KIT, TET1 and TET2 gene expression in Acute Myeloid Leukemia.Molecular biology reports · 2023Article
- Role of TET dioxygenases in the regulation of both normal and pathological hematopoiesis.Journal of experimental & clinical cancer research : CR · 2022Review
- Protocol to establish a stableSTAR protocols · 2022Article
- TET3 promotes AML growth and epigenetically regulates glucose metabolism and leukemic stem cell associated pathways.Leukemia · 2022Article
- ZNF521 Enhances MLL-AF9-Dependent Hematopoietic Stem Cell Transformation in Acute Myeloid Leukemias by Altering the Gene Expression Landscape.International journal of molecular sciences · 2021Article
- Integrated bioinformatics analysis revealed the regulation of angiogenesis by tumor cells in hepatocellular carcinoma.Bioscience reports · 2021Article
- Ten-Eleven Translocation 1 Promotes Malignant Progression of Cholangiocarcinoma With Wild-Type Isocitrate Dehydrogenase 1.Hepatology (Baltimore, Md.) · 2021Article
Corrections and comments
- Erratum issued
Authors and funding
34 authors at 10 institutions in 2 countries.
Xi JiangDepartment of Cancer Biology, University of Cincinnati, Cincinnati, OH, 45219, USA. xjiang@coh.org.
Chao HuDepartment of Cancer Biology, University of Cincinnati, Cincinnati, OH, 45219, USA.
Kyle FerchenDepartment of Cancer Biology, University of Cincinnati, Cincinnati, OH, 45219, USA.
Ji NieDepartment of Chemistry, Department of Biochemistry and Molecular Biology, Institute for Biophysical Dynamics, Howard Hughes Medical Institute, University of Chicago, Chicago, IL, 60637, USA.
Xiaolong CuiDepartment of Chemistry, Department of Biochemistry and Molecular Biology, Institute for Biophysical Dynamics, Howard Hughes Medical Institute, University of Chicago, Chicago, IL, 60637, USA.
Chih-Hong ChenDepartment of Molecular Medicine, Beckman Research Institute of City of Hope, Duarte, CA, 91010, USA.
Liting ChengKey Laboratory of Luminescence and Real-time Analytical Chemistry (Ministry of Education), College of Pharmaceutical Sciences, Southwest University, Chongqing, 400715, China.
Zhixiang ZuoDepartment of Cancer Biology, University of Cincinnati, Cincinnati, OH, 45219, USA.
William SeibelDivision of Oncology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, 45229, USA.
Chunjiang HeSchool of Basic Medical Sciences, Wuhan University, Wuhan, 430071, China.
Yixuan TangKey Laboratory of Luminescence and Real-time Analytical Chemistry (Ministry of Education), College of Pharmaceutical Sciences, Southwest University, Chongqing, 400715, China.
Jennifer R SkibbeDepartment of Cancer Biology, University of Cincinnati, Cincinnati, OH, 45219, USA.
Mark WunderlichExperimental Hematology and Cancer Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, 45229, USA.
William C ReinholdDevelopmental Therapeutics Branch, Center for Cancer Research, NCI, NIH, Bethesda, MD, 20892, USA.
Lei DongDepartment of Cancer Biology, University of Cincinnati, Cincinnati, OH, 45219, USA.
Chao ShenDepartment of Cancer Biology, University of Cincinnati, Cincinnati, OH, 45219, USA.
Stephen ArnovitzSection of Hematology/Oncology, Department of Medicine, University of Chicago, Chicago, IL, 60637, USA.
Bryan UlrichSection of Hematology/Oncology, Department of Medicine, University of Chicago, Chicago, IL, 60637, USA.
Jiuwei LuDepartment of Cancer Biology, University of Cincinnati, Cincinnati, OH, 45219, USA.
Hengyou WengDepartment of Cancer Biology, University of Cincinnati, Cincinnati, OH, 45219, USA.
Rui SuDepartment of Cancer Biology, University of Cincinnati, Cincinnati, OH, 45219, USA.
Huilin HuangDepartment of Cancer Biology, University of Cincinnati, Cincinnati, OH, 45219, USA.
Yungui WangDepartment of Cancer Biology, University of Cincinnati, Cincinnati, OH, 45219, USA.
Chenying LiDepartment of Cancer Biology, University of Cincinnati, Cincinnati, OH, 45219, USA.
Xi QinDepartment of Cancer Biology, University of Cincinnati, Cincinnati, OH, 45219, USA.
James C MulloyExperimental Hematology and Cancer Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, 45229, USA.
Yi ZhengExperimental Hematology and Cancer Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, 45229, USA.
Jiajie DiaoDepartment of Cancer Biology, University of Cincinnati, Cincinnati, OH, 45219, USA.ORCID http://orcid.org/0000-0003-4288-3203
Jie JinDepartment of Hematology, The First Affiliated Hospital, Zhejiang University, Hangzhou, Zhejiang, 310003, China.
Chong LiKey Laboratory of Luminescence and Real-time Analytical Chemistry (Ministry of Education), College of Pharmaceutical Sciences, Southwest University, Chongqing, 400715, China.
Paul P LiuGenetics and Molecular Biology Branch, National Human Genome Research Institute, NIH, Bethesda, MD, 20892, USA.
Chuan HeDepartment of Chemistry, Department of Biochemistry and Molecular Biology, Institute for Biophysical Dynamics, Howard Hughes Medical Institute, University of Chicago, Chicago, IL, 60637, USA.
Yuan ChenDepartment of Molecular Medicine, Beckman Research Institute of City of Hope, Duarte, CA, 91010, USA.
Jianjun ChenDepartment of Cancer Biology, University of Cincinnati, Cincinnati, OH, 45219, USA. jianchen@coh.org.
City of Hope · USUniversity of Chicago · USCincinnati Children's Hospital Medical Center · USHoward Hughes Medical Institute · USSouthwest University · CNUniversity of Cincinnati · USCenter for Cancer Research · USFirst Affiliated Hospital Zhejiang University · CNNational Human Genome Research Institute · USSun Yat-sen University · CN
Funding
Transcriptome-wide base-resolution sequencing of pseudouridine in human normal and AD brain tissues-CEGS Admin supplement 2020-2021RM1HG008935 · NHGRI · UNIVERSITY OF CHICAGO · PI HE, CHUAN · 2016 to 2025
$24.4MMOLECULAR PATHOGENESIS OF CHROMOSOME 16 INVERSION INHUMAN LEUKEMIAZIAHG000030 · NHGRI · NATIONAL HUMAN GENOME RESEARCH INSTITUTE · PI LIU, PAUL · 2009 to 2025
$15.8MMulti-Disciplinary Training Grant in Cancer ResearchT32CA009594 · NCI · UNIVERSITY OF CHICAGO · PI KAY F MACLEOD, Scott A. Oakes · 1989 to 2026
$11.5MSUMO modification and DNA damage response in cancer therapyR01GM086171 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI CHEN, YUAN · 2008 to 2020
$5.2MTargeting c-Myc and Proteasome Inhibitor Resistance in Multiple MyelomaR01CA212119 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI CHEN, YUAN · 2017 to 2021
$2.8MTargeting TET1 signaling to treat acute myeloid leukemiaR01CA211614 · NCI · UNIVERSITY OF CINCINNATI · PI CHEN, JIANJUN · 2017 to 2021
$2.3MThe role and mechanism of FTO in leukemogenesis and drug responseR01CA214965 · NCI · UNIVERSITY OF CINCINNATI · PI CHEN, JIANJUN · 2017 to 2021
$2.1MTherapeutic insights through patient derived leukemia xenograftsR50CA211404 · NCI · CINCINNATI CHILDRENS HOSP MED CTR · PI Mark Wunderlich · 2016 to 2026
$1.9MPotential therapeutic implications of targeting miR-150 in acute myeloid leukemiaR01CA182528 · NCI · UNIVERSITY OF CINCINNATI · PI CHEN, JIANJUN · 2014 to 2018
$1.7MThe role and functional mechanism of TET1 in MLL-rearranged leukemiaR01CA178454 · NCI · UNIVERSITY OF CINCINNATI · PI CHEN, JIANJUN · 2014 to 2018
$1.7MThe role and functional mechanism of a miRNA cluster, mir-17-92 in leukemogenesisR01CA127277 · NCI · UNIVERSITY OF CHICAGO · PI CHEN, JIANJUN · 2008 to 2012
$1.4MHoward Hughes Medical InstituteNCI NIH HHS R01 CA127277NCI NIH HHS R01 CA178454NCI NIH HHS R01 CA182528NCI NIH HHS R01 CA211614NCI NIH HHS R01 CA212119NCI NIH HHS R01 CA214965NCI NIH HHS R50 CA211404NCI NIH HHS T32 CA009594NHGRI NIH HHS RM1 HG008935NIGMS NIH HHS R01 GM086171
Abstract
Effective therapy of acute myeloid leukemia (AML) remains an unmet need. DNA methylcytosine dioxygenase Ten-eleven translocation 1 (TET1) is a critical oncoprotein in AML. Through a series of data analysis and drug screening, we identified two compounds (i.e., NSC-311068 and NSC-370284) that selectively suppress TET1 transcription and 5-hydroxymethylcytosine (5hmC) modification, and effectively inhibit cell viability in AML with high expression of TET1 (i.e., TET1-high AML), including AML carrying t(11q23)/MLL-rearrangements and t(8;21) AML. NSC-311068 and especially NSC-370284 significantly repressed TET1-high AML progression in vivo. UC-514321, a structural analog of NSC-370284, exhibited a more potent therapeutic effect and prolonged the median survival of TET1-high AML mice over three fold. NSC-370284 and UC-514321 both directly target STAT3/5, transcriptional activators of TET1, and thus repress TET1 expression. They also exhibit strong synergistic effects with standard chemotherapy. Our results highlight the therapeutic potential of targeting the STAT/TET1 axis by selective inhibitors in AML treatment.
Indexed as
AnimalsAntineoplastic Combined Chemotherapy ProtocolsCell Line, TumorDaunorubicinEnzyme InhibitorsGene Expression Regulation, LeukemicHumansKaplan-Meier EstimateLeukemia, ExperimentalLeukemia, Myeloid, AcuteMice, Inbred C57BLMixed Function OxygenasesProto-Oncogene ProteinsRNA InterferenceSTAT3 Transcription FactorSTAT5 Transcription FactorDaunorubicinEnzyme InhibitorsMixed Function OxygenasesProto-Oncogene ProteinsSTAT3 Transcription FactorSTAT5 Transcription FactorTET1 protein, human
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