miR-22 has a potent anti-tumour role with therapeutic potential in acute myeloid leukaemia

MicroRNAs are subject to precise regulation and have key roles in tumorigenesis. In contrast to the oncogenic role of miR-22 reported in myelodysplastic syndrome (MDS) and breast cancer, here we show that miR-22 is an essential anti-tumour gatekeeper in de novo acute myeloid leukaemia (AML) where it...

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Vydáno v:Nature communications Ročník 7; číslo 1; s. 11452
Hlavní autoři: Jiang, Xi, Hu, Chao, Arnovitz, Stephen, Bugno, Jason, Yu, Miao, Zuo, Zhixiang, Chen, Ping, Huang, Hao, Ulrich, Bryan, Gurbuxani, Sandeep, Weng, Hengyou, Strong, Jennifer, Wang, Yungui, Li, Yuanyuan, Salat, Justin, Li, Shenglai, Elkahloun, Abdel G., Yang, Yang, Neilly, Mary Beth, Larson, Richard A., Le Beau, Michelle M., Herold, Tobias, Bohlander, Stefan K., Liu, Paul P., Zhang, Jiwang, Li, Zejuan, He, Chuan, Jin, Jie, Hong, Seungpyo, Chen, Jianjun
Médium: Journal Article
Jazyk:angličtina
Vydáno: London Nature Publishing Group UK 26.04.2016
Nature Publishing Group
Nature Portfolio
Témata:
13
14
38
631/337/384/331
631/67/1059
631/67/1990/283/1897
631/80/86
64
96
Acute Disease
Animals
Breast cancer
Cell Line
Cell Line, Tumor
Cell Proliferation - genetics
Down-Regulation
Epigenesis, Genetic
Epigenetics
Gene Expression Profiling
Gene Expression Regulation, Leukemic
Genes, Tumor Suppressor
HEK293 Cells
Hematology
Humanities and Social Sciences
Humans
Leukemia
Leukemia, Myeloid - drug therapy
Leukemia, Myeloid - genetics
Leukemia, Myeloid - pathology
Medicine
Mice, Inbred C57BL
MicroRNAs
MicroRNAs - chemistry
MicroRNAs - genetics
MicroRNAs - therapeutic use
multidisciplinary
Mutation
Myelodysplastic syndromes
Myelodysplastic Syndromes - genetics
Myelodysplastic Syndromes - pathology
Oncology
Pathogenesis
Roles
Science
Science (multidisciplinary)
Signal Transduction - genetics
Chicago Illinois
United States > US
Illinois
China
ISSN:2041-1723, 2041-1723
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Abstract MicroRNAs are subject to precise regulation and have key roles in tumorigenesis. In contrast to the oncogenic role of miR-22 reported in myelodysplastic syndrome (MDS) and breast cancer, here we show that miR-22 is an essential anti-tumour gatekeeper in de novo acute myeloid leukaemia (AML) where it is significantly downregulated. Forced expression of miR-22 significantly suppresses leukaemic cell viability and growth in vitro , and substantially inhibits leukaemia development and maintenance in vivo . Mechanistically, miR-22 targets multiple oncogenes, including CRTC1 , FLT3 and MYCBP , and thus represses the CREB and MYC pathways. The downregulation of miR-22 in AML is caused by TET1/GFI1/EZH2/SIN3A-mediated epigenetic repression and/or DNA copy-number loss. Furthermore, nanoparticles carrying miR-22 oligos significantly inhibit leukaemia progression in vivo . Together, our study uncovers a TET1/GFI1/EZH2/SIN3A/miR-22/CREB-MYC signalling circuit and thereby provides insights into epigenetic/genetic mechanisms underlying the pathogenesis of AML, and also highlights the clinical potential of miR-22-based AML therapy. Mir-22 has been shown to be an oncogenic microRNA in breast cancer and myelodysplastic syndrome. Here, the authors show that mir-22 functions as a tumour suppressor in de novo acute myeloid leukaemia by inhibiting the expression of several oncogenes and that restoring mir-22 expression suppresses AML progression.
AbstractList MicroRNAs are subject to precise regulation and have key roles in tumorigenesis. In contrast to the oncogenic role of miR-22 reported in myelodysplastic syndrome (MDS) and breast cancer, here we show that miR-22 is an essential anti-tumour gatekeeper in de novo acute myeloid leukaemia (AML) where it is significantly downregulated. Forced expression of miR-22 significantly suppresses leukaemic cell viability and growth in vitro, and substantially inhibits leukaemia development and maintenance in vivo. Mechanistically, miR-22 targets multiple oncogenes, including CRTC1, FLT3 and MYCBP, and thus represses the CREB and MYC pathways. The downregulation of miR-22 in AML is caused by TET1/GFI1/EZH2/SIN3A-mediated epigenetic repression and/or DNA copy-number loss. Furthermore, nanoparticles carrying miR-22 oligos significantly inhibit leukaemia progression in vivo. Together, our study uncovers a TET1/GFI1/EZH2/SIN3A/miR-22/CREB-MYC signalling circuit and thereby provides insights into epigenetic/genetic mechanisms underlying the pathogenesis of AML, and also highlights the clinical potential of miR-22-based AML therapy. Mir-22 has been shown to be an oncogenic microRNA in breast cancer and myelodysplastic syndrome. Here, the authors show that mir-22 functions as a tumour suppressor in de novo acute myeloid leukaemia by inhibiting the expression of several oncogenes and that restoring mir-22 expression suppresses AML progression.
MicroRNAs are subject to precise regulation and have key roles in tumorigenesis. In contrast to the oncogenic role of miR-22 reported in myelodysplastic syndrome (MDS) and breast cancer, here we show that miR-22 is an essential anti-tumour gatekeeper in de novo acute myeloid leukaemia (AML) where it is significantly downregulated. Forced expression of miR-22 significantly suppresses leukaemic cell viability and growth in vitro, and substantially inhibits leukaemia development and maintenance in vivo. Mechanistically, miR-22 targets multiple oncogenes, including CRTC1, FLT3 and MYCBP, and thus represses the CREB and MYC pathways. The downregulation of miR-22 in AML is caused by TET1/GFI1/EZH2/SIN3A-mediated epigenetic repression and/or DNA copy-number loss. Furthermore, nanoparticles carrying miR-22 oligos significantly inhibit leukaemia progression in vivo. Together, our study uncovers a TET1/GFI1/EZH2/SIN3A/miR-22/CREB-MYC signalling circuit and thereby provides insights into epigenetic/genetic mechanisms underlying the pathogenesis of AML, and also highlights the clinical potential of miR-22-based AML therapy.
MicroRNAs are subject to precise regulation and have key roles in tumorigenesis. In contrast to the oncogenic role of miR-22 reported in myelodysplastic syndrome (MDS) and breast cancer, here we show that miR-22 is an essential anti-tumour gatekeeper in de novo acute myeloid leukaemia (AML) where it is significantly downregulated. Forced expression of miR-22 significantly suppresses leukaemic cell viability and growth in vitro , and substantially inhibits leukaemia development and maintenance in vivo . Mechanistically, miR-22 targets multiple oncogenes, including CRTC1 , FLT3 and MYCBP , and thus represses the CREB and MYC pathways. The downregulation of miR-22 in AML is caused by TET1/GFI1/EZH2/SIN3A-mediated epigenetic repression and/or DNA copy-number loss. Furthermore, nanoparticles carrying miR-22 oligos significantly inhibit leukaemia progression in vivo . Together, our study uncovers a TET1/GFI1/EZH2/SIN3A/miR-22/CREB-MYC signalling circuit and thereby provides insights into epigenetic/genetic mechanisms underlying the pathogenesis of AML, and also highlights the clinical potential of miR-22-based AML therapy.
Mir-22 has been shown to be an oncogenic microRNA in breast cancer and myelodysplastic syndrome. Here, the authors show that mir-22 functions as a tumour suppressor in de novoacute myeloid leukaemia by inhibiting the expression of several oncogenes and that restoring mir-22 expression suppresses AML progression.
MicroRNAs are subject to precise regulation and have key roles in tumorigenesis. In contrast to the oncogenic role of miR-22 reported in myelodysplastic syndrome (MDS) and breast cancer, here we show that miR-22 is an essential anti-tumour gatekeeper in de novo acute myeloid leukaemia (AML) where it is significantly downregulated. Forced expression of miR-22 significantly suppresses leukaemic cell viability and growth in vitro , and substantially inhibits leukaemia development and maintenance in vivo . Mechanistically, miR-22 targets multiple oncogenes, including CRTC1 , FLT3 and MYCBP , and thus represses the CREB and MYC pathways. The downregulation of miR-22 in AML is caused by TET1/GFI1/EZH2/SIN3A-mediated epigenetic repression and/or DNA copy-number loss. Furthermore, nanoparticles carrying miR-22 oligos significantly inhibit leukaemia progression in vivo . Together, our study uncovers a TET1/GFI1/EZH2/SIN3A/miR-22/CREB-MYC signalling circuit and thereby provides insights into epigenetic/genetic mechanisms underlying the pathogenesis of AML, and also highlights the clinical potential of miR-22-based AML therapy. Mir-22 has been shown to be an oncogenic microRNA in breast cancer and myelodysplastic syndrome. Here, the authors show that mir-22 functions as a tumour suppressor in de novo acute myeloid leukaemia by inhibiting the expression of several oncogenes and that restoring mir-22 expression suppresses AML progression.
ArticleNumber 11452
Author Li, Yuanyuan
Bohlander, Stefan K.
Hu, Chao
Salat, Justin
Jin, Jie
Zhang, Jiwang
Strong, Jennifer
Neilly, Mary Beth
Le Beau, Michelle M.
Bugno, Jason
Yu, Miao
Gurbuxani, Sandeep
Li, Shenglai
Arnovitz, Stephen
He, Chuan
Larson, Richard A.
Yang, Yang
Hong, Seungpyo
Ulrich, Bryan
Elkahloun, Abdel G.
Herold, Tobias
Chen, Ping
Jiang, Xi
Zuo, Zhixiang
Liu, Paul P.
Huang, Hao
Chen, Jianjun
Li, Zejuan
Wang, Yungui
Weng, Hengyou
Author_xml – sequence: 1
  givenname: Xi
  surname: Jiang
  fullname: Jiang, Xi
  organization: Department of Cancer Biology, University of Cincinnati, Department of Medicine, Section of Hematology/Oncology, University of Chicago
– sequence: 2
  givenname: Chao
  surname: Hu
  fullname: Hu, Chao
  organization: Department of Cancer Biology, University of Cincinnati, Department of Medicine, Section of Hematology/Oncology, University of Chicago, Department of Hematology, The First Affiliated Hospital Zhejiang University
– sequence: 3
  givenname: Stephen
  surname: Arnovitz
  fullname: Arnovitz, Stephen
  organization: Department of Medicine, Section of Hematology/Oncology, University of Chicago
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  givenname: Jason
  surname: Bugno
  fullname: Bugno, Jason
  organization: Department of Biopharmaceutical Sciences College of Pharmacy, The University of Illinois
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  givenname: Miao
  surname: Yu
  fullname: Yu, Miao
  organization: Department of Chemistry and Institute for Biophysical Dynamics, Howard Hughes Medical Institute, University of Chicago
– sequence: 6
  givenname: Zhixiang
  surname: Zuo
  fullname: Zuo, Zhixiang
  organization: Department of Cancer Biology, University of Cincinnati, Department of Medicine, Section of Hematology/Oncology, University of Chicago, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center
– sequence: 7
  givenname: Ping
  surname: Chen
  fullname: Chen, Ping
  organization: Department of Medicine, Section of Hematology/Oncology, University of Chicago
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  surname: Huang
  fullname: Huang, Hao
  organization: Department of Medicine, Section of Hematology/Oncology, University of Chicago
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  surname: Ulrich
  fullname: Ulrich, Bryan
  organization: Department of Medicine, Section of Hematology/Oncology, University of Chicago
– sequence: 10
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  surname: Gurbuxani
  fullname: Gurbuxani, Sandeep
  organization: Department of Pathology, University of Chicago
– sequence: 11
  givenname: Hengyou
  surname: Weng
  fullname: Weng, Hengyou
  organization: Department of Cancer Biology, University of Cincinnati, Department of Medicine, Section of Hematology/Oncology, University of Chicago
– sequence: 12
  givenname: Jennifer
  surname: Strong
  fullname: Strong, Jennifer
  organization: Department of Cancer Biology, University of Cincinnati
– sequence: 13
  givenname: Yungui
  surname: Wang
  fullname: Wang, Yungui
  organization: Department of Cancer Biology, University of Cincinnati, Department of Medicine, Section of Hematology/Oncology, University of Chicago, Department of Hematology, The First Affiliated Hospital Zhejiang University
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  givenname: Yuanyuan
  surname: Li
  fullname: Li, Yuanyuan
  organization: Department of Medicine, Section of Hematology/Oncology, University of Chicago
– sequence: 15
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  surname: Salat
  fullname: Salat, Justin
  organization: Department of Medicine, Section of Hematology/Oncology, University of Chicago
– sequence: 16
  givenname: Shenglai
  surname: Li
  fullname: Li, Shenglai
  organization: Department of Medicine, Section of Hematology/Oncology, University of Chicago
– sequence: 17
  givenname: Abdel G.
  surname: Elkahloun
  fullname: Elkahloun, Abdel G.
  organization: Division of Intramural Research, National Human Genome Research Institute, NIH
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  surname: Yang
  fullname: Yang, Yang
  organization: Department of Biopharmaceutical Sciences College of Pharmacy, The University of Illinois
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  surname: Neilly
  fullname: Neilly, Mary Beth
  organization: Department of Medicine, Section of Hematology/Oncology, University of Chicago
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  surname: Larson
  fullname: Larson, Richard A.
  organization: Department of Medicine, Section of Hematology/Oncology, University of Chicago
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  givenname: Michelle M.
  surname: Le Beau
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  organization: Department of Medicine, Section of Hematology/Oncology, University of Chicago
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  surname: Herold
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  organization: Department of Internal Medicine 3, University Hospital Grosshadern, Ludwig-Maximilians-Universität
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  givenname: Stefan K.
  surname: Bohlander
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  organization: Department of Molecular Medicine and Pathology, University of Auckland
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  organization: Oncology Institute, Cardinal Bernardin Cancer Center, Loyola University Medical Center
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  givenname: Chuan
  surname: He
  fullname: He, Chuan
  organization: Department of Chemistry and Institute for Biophysical Dynamics, Howard Hughes Medical Institute, University of Chicago
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  givenname: Jie
  surname: Jin
  fullname: Jin, Jie
  organization: Department of Hematology, The First Affiliated Hospital Zhejiang University
– sequence: 29
  givenname: Seungpyo
  surname: Hong
  fullname: Hong, Seungpyo
  organization: Department of Biopharmaceutical Sciences College of Pharmacy, The University of Illinois, Integrated Science and Engineering Division, Underwood International College, Yonsei University
– sequence: 30
  givenname: Jianjun
  surname: Chen
  fullname: Chen, Jianjun
  email: chen3jj@ucmail.uc.edu
  organization: Department of Cancer Biology, University of Cincinnati, Department of Medicine, Section of Hematology/Oncology, University of Chicago
BackLink https://www.ncbi.nlm.nih.gov/pubmed/27116251$$D View this record in MEDLINE/PubMed
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ContentType Journal Article
Copyright The Author(s) 2016
Copyright Nature Publishing Group Apr 2016
Copyright © 2016, Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved. 2016 Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved.
Copyright_xml – notice: The Author(s) 2016
– notice: Copyright Nature Publishing Group Apr 2016
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Snippet MicroRNAs are subject to precise regulation and have key roles in tumorigenesis. In contrast to the oncogenic role of miR-22 reported in myelodysplastic...
Mir-22 has been shown to be an oncogenic microRNA in breast cancer and myelodysplastic syndrome. Here, the authors show that mir-22 functions as a tumour...
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StartPage 11452
SubjectTerms 13
14
38
631/337/384/331
631/67/1059
631/67/1990/283/1897
631/80/86
64
96
Acute Disease
Animals
Breast cancer
Cell Line
Cell Line, Tumor
Cell Proliferation - genetics
Down-Regulation
Epigenesis, Genetic
Epigenetics
Gene Expression Profiling
Gene Expression Regulation, Leukemic
Genes, Tumor Suppressor
HEK293 Cells
Hematology
Humanities and Social Sciences
Humans
Leukemia
Leukemia, Myeloid - drug therapy
Leukemia, Myeloid - genetics
Leukemia, Myeloid - pathology
Medicine
Mice, Inbred C57BL
MicroRNAs
MicroRNAs - chemistry
MicroRNAs - genetics
MicroRNAs - therapeutic use
multidisciplinary
Mutation
Myelodysplastic syndromes
Myelodysplastic Syndromes - genetics
Myelodysplastic Syndromes - pathology
Oncology
Pathogenesis
Roles
Science
Science (multidisciplinary)
Signal Transduction - genetics
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Title miR-22 has a potent anti-tumour role with therapeutic potential in acute myeloid leukaemia
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