Nature Communications (Dec 2017)
Targeted inhibition of STAT/TET1 axis as a therapeutic strategy for acute myeloid leukemia
- Xi Jiang,
- Chao Hu,
- Kyle Ferchen,
- Ji Nie,
- Xiaolong Cui,
- Chih-Hong Chen,
- Liting Cheng,
- Zhixiang Zuo,
- William Seibel,
- Chunjiang He,
- Yixuan Tang,
- Jennifer R. Skibbe,
- Mark Wunderlich,
- William C. Reinhold,
- Lei Dong,
- Chao Shen,
- Stephen Arnovitz,
- Bryan Ulrich,
- Jiuwei Lu,
- Hengyou Weng,
- Rui Su,
- Huilin Huang,
- Yungui Wang,
- Chenying Li,
- Xi Qin,
- James C. Mulloy,
- Yi Zheng,
- Jiajie Diao,
- Jie Jin,
- Chong Li,
- Paul P. Liu,
- Chuan He,
- Yuan Chen,
- Jianjun Chen
Affiliations
- Xi Jiang
- Department of Cancer Biology, University of Cincinnati
- Chao Hu
- Department of Cancer Biology, University of Cincinnati
- Kyle Ferchen
- Department of Cancer Biology, University of Cincinnati
- Ji Nie
- Department of Chemistry, Department of Biochemistry and Molecular Biology, Institute for Biophysical Dynamics, Howard Hughes Medical Institute, University of Chicago
- Xiaolong Cui
- Department of Chemistry, Department of Biochemistry and Molecular Biology, Institute for Biophysical Dynamics, Howard Hughes Medical Institute, University of Chicago
- Chih-Hong Chen
- Department of Molecular Medicine, Beckman Research Institute of City of Hope
- Liting Cheng
- Key Laboratory of Luminescence and Real-time Analytical Chemistry (Ministry of Education), College of Pharmaceutical Sciences, Southwest University
- Zhixiang Zuo
- Department of Cancer Biology, University of Cincinnati
- William Seibel
- Division of Oncology, Cincinnati Children’s Hospital Medical Center
- Chunjiang He
- School of Basic Medical Sciences, Wuhan University
- Yixuan Tang
- Key Laboratory of Luminescence and Real-time Analytical Chemistry (Ministry of Education), College of Pharmaceutical Sciences, Southwest University
- Jennifer R. Skibbe
- Department of Cancer Biology, University of Cincinnati
- Mark Wunderlich
- Experimental Hematology and Cancer Biology, Cincinnati Children’s Hospital Medical Center
- William C. Reinhold
- Developmental Therapeutics Branch, Center for Cancer Research, NCI, NIH
- Lei Dong
- Department of Cancer Biology, University of Cincinnati
- Chao Shen
- Department of Cancer Biology, University of Cincinnati
- Stephen Arnovitz
- Section of Hematology/Oncology, Department of Medicine, University of Chicago
- Bryan Ulrich
- Section of Hematology/Oncology, Department of Medicine, University of Chicago
- Jiuwei Lu
- Department of Cancer Biology, University of Cincinnati
- Hengyou Weng
- Department of Cancer Biology, University of Cincinnati
- Rui Su
- Department of Cancer Biology, University of Cincinnati
- Huilin Huang
- Department of Cancer Biology, University of Cincinnati
- Yungui Wang
- Department of Cancer Biology, University of Cincinnati
- Chenying Li
- Department of Cancer Biology, University of Cincinnati
- Xi Qin
- Department of Cancer Biology, University of Cincinnati
- James C. Mulloy
- Experimental Hematology and Cancer Biology, Cincinnati Children’s Hospital Medical Center
- Yi Zheng
- Experimental Hematology and Cancer Biology, Cincinnati Children’s Hospital Medical Center
- Jiajie Diao
- Department of Cancer Biology, University of Cincinnati
- Jie Jin
- Department of Hematology, The First Affiliated Hospital, Zhejiang University
- Chong Li
- Key Laboratory of Luminescence and Real-time Analytical Chemistry (Ministry of Education), College of Pharmaceutical Sciences, Southwest University
- Paul P. Liu
- Genetics and Molecular Biology Branch, National Human Genome Research Institute, NIH
- Chuan He
- Department of Chemistry, Department of Biochemistry and Molecular Biology, Institute for Biophysical Dynamics, Howard Hughes Medical Institute, University of Chicago
- Yuan Chen
- Department of Molecular Medicine, Beckman Research Institute of City of Hope
- Jianjun Chen
- Department of Cancer Biology, University of Cincinnati
- DOI
- https://doi.org/10.1038/s41467-017-02290-w
- Journal volume & issue
-
Vol. 8,
no. 1
pp. 1 – 13
Abstract
Ten-eleven translocation 1 (TET1) is a critical oncoprotein in AML. Here, the authors identify 2 compounds that target the binding of STAT3/5 specifically to the TET1 promoter, inhibiting its expression and AML cell viability.
