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microRNA-452 exerts growth-suppressive activity against T-cell acute lymphoblastic leukemia

Haihao Wang, Qiannan Guo, Guizhi Zhu, Shuo Zhu, Peiwen Yang, Mingsheng Zhang
DOI: 10.1136/jim-2017-000591 Published 5 April 2018
Haihao Wang
1 Department of Cardiovascular Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
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Qiannan Guo
1 Department of Cardiovascular Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
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Guizhi Zhu
1 Department of Cardiovascular Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
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Shuo Zhu
1 Department of Cardiovascular Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
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Peiwen Yang
2 Reproductive Medicine Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
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Mingsheng Zhang
3 Department of Oncology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
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Abstract

T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematological cancer. Although microRNA (miR)-452 serves as a tumor suppressor in multiple solid tumors, its expression and function in hematological cancers including T-ALL is largely unknown. We measured the expression of miR-452 in 38 T-ALL and 22 normal lymph node samples by real-time PCR analysis. The methylation levels in the promoter of miR-452 were determined using MethyLight assay. The effects of miR-452 overexpression on proliferation, cell cycle distribution, and tumorigenesis were explored. It was found that miR-452 expression levels were significantly lower in T-ALL specimens than in normal lymph node biopsies (P=0.0079). T-ALL specimens had a significantly higher methylation level in the promoter of miR-452 than normal lymph node tissues (P=0.0014). Consistently, miR-452 was downregulated in Jurkat and Molt-4 T-ALL cells, whose expression was restored after treatment with a demethylation agent 5-aza-2′-deoxycytidine. Ectopic expression of miR-452 inhibited the proliferation of Jurkat and Molt-4 cells and induced a G0/G1 cell cycle arrest. Overexpression of miR-452 suppressed the protein expression of BMI1 in T-ALL cells. Rescue experiments revealed that overexpression of BMI1 partially reversed the growth-suppressive effect of miR-452 on T-ALL cells. Xenograft tumor studies confirmed that overexpression of miR-452 suppressed tumor growth in nude mice and reduced the expression of BMI1. Collectively, miR-452 is epigenetically silenced and targets BMI1 to exert a growth suppressive activity in T-ALL. Restoration of miR-452 expression may represent a promising therapeutic strategy for this malignancy.

Footnotes

  • Contributors SZ and PY participated in study design in vitro experiments. HW, QG, GZ, and MZ participated in study design, in vitro experiments, in vivo experiments, and drafting of the manuscript.

  • Competing interests None declared.

  • Patient consent Obtained.

  • Ethics approval Institutional Review Board of Huazhong University of Science and Technology (Wuhan, China).

  • Provenance and peer review Not commissioned; externally peer reviewed.

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Vol 66 Issue 4 Table of Contents
Journal of Investigative Medicine: 66 (4)
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microRNA-452 exerts growth-suppressive activity against T-cell acute lymphoblastic leukemia
Haihao Wang, Qiannan Guo, Guizhi Zhu, Shuo Zhu, Peiwen Yang, Mingsheng Zhang
Journal of Investigative Medicine Apr 2018, 66 (4) 773-779; DOI: 10.1136/jim-2017-000591

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microRNA-452 exerts growth-suppressive activity against T-cell acute lymphoblastic leukemia
Haihao Wang, Qiannan Guo, Guizhi Zhu, Shuo Zhu, Peiwen Yang, Mingsheng Zhang
Journal of Investigative Medicine Apr 2018, 66 (4) 773-779; DOI: 10.1136/jim-2017-000591
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microRNA-452 exerts growth-suppressive activity against T-cell acute lymphoblastic leukemia
Haihao Wang, Qiannan Guo, Guizhi Zhu, Shuo Zhu, Peiwen Yang, Mingsheng Zhang
Journal of Investigative Medicine Apr 2018, 66 (4) 773-779; DOI: 10.1136/jim-2017-000591
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