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miR-221-3p Delivered by BMMSC-Derived Microvesicles Promotes the Development of Acute Myelocytic Leukemia

Objective: The study aims to investigate the effects of miR-221-3p in bone marrow mesenchymal stem cell (BMMSC)-derived microvesicles (MVs) on cell cycle, proliferation and invasion of acute myelocytic leukemia (AML). Methods: Bioinformatics was used to predict differentially expressed miRNAs (DEmiR...

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Autores principales: Zhang, Xuewu, Xu, Yu, Wang, Jinghan, Zhao, Shuqi, Li, Jianhu, Huang, Xin, Xu, Huan, Zhang, Xiang, Suo, Shanshan, Lv, Yunfei, Zhang, Yi, Yu, Wenjuan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7033425/
https://www.ncbi.nlm.nih.gov/pubmed/32117949
http://dx.doi.org/10.3389/fbioe.2020.00081
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author Zhang, Xuewu
Xu, Yu
Wang, Jinghan
Zhao, Shuqi
Li, Jianhu
Huang, Xin
Xu, Huan
Zhang, Xiang
Suo, Shanshan
Lv, Yunfei
Zhang, Yi
Yu, Wenjuan
author_facet Zhang, Xuewu
Xu, Yu
Wang, Jinghan
Zhao, Shuqi
Li, Jianhu
Huang, Xin
Xu, Huan
Zhang, Xiang
Suo, Shanshan
Lv, Yunfei
Zhang, Yi
Yu, Wenjuan
author_sort Zhang, Xuewu
collection PubMed
description Objective: The study aims to investigate the effects of miR-221-3p in bone marrow mesenchymal stem cell (BMMSC)-derived microvesicles (MVs) on cell cycle, proliferation and invasion of acute myelocytic leukemia (AML). Methods: Bioinformatics was used to predict differentially expressed miRNAs (DEmiRNAs) in AML. The morphology of BMMSC-derived MVs was observed under an electron microscope, and the positional relation of MVs and OCI-AML2 cells was observed by a fluorescence microscope. MTT, Transwell, and flow cytometry assays were used to analyze the effects of MVs on OCI-AML2 cells. The targeted relationship between miR-221-3p and CDKN1C was detected by dual luciferase assay. Results: It was verified that miR-221-3p promoted the proliferation, invasion and migration of OCI-AML2 cells, and induced the cell cycle arrest in G1/S phase as well as inhibited cell apoptosis. Further studies showed that MVs promoted the proliferation, migration and invasion of AML, and induced the cell cycle arrest in G1/S phase through miR-221-3p. It was confirmed that miR-221-3p can directly target CDKN1C to regulate cell cycle, proliferation and invasion of AML. Conclusion: miR-221-3p in BMMSC-derived MVs regulated AML cell cycle, cell proliferation and invasion through targeting CDKN1C. miR-221-3p and CDKN1C were considered to be potential targets and biomarkers for the treatment of AML in clinic.
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spelling pubmed-70334252020-02-28 miR-221-3p Delivered by BMMSC-Derived Microvesicles Promotes the Development of Acute Myelocytic Leukemia Zhang, Xuewu Xu, Yu Wang, Jinghan Zhao, Shuqi Li, Jianhu Huang, Xin Xu, Huan Zhang, Xiang Suo, Shanshan Lv, Yunfei Zhang, Yi Yu, Wenjuan Front Bioeng Biotechnol Bioengineering and Biotechnology Objective: The study aims to investigate the effects of miR-221-3p in bone marrow mesenchymal stem cell (BMMSC)-derived microvesicles (MVs) on cell cycle, proliferation and invasion of acute myelocytic leukemia (AML). Methods: Bioinformatics was used to predict differentially expressed miRNAs (DEmiRNAs) in AML. The morphology of BMMSC-derived MVs was observed under an electron microscope, and the positional relation of MVs and OCI-AML2 cells was observed by a fluorescence microscope. MTT, Transwell, and flow cytometry assays were used to analyze the effects of MVs on OCI-AML2 cells. The targeted relationship between miR-221-3p and CDKN1C was detected by dual luciferase assay. Results: It was verified that miR-221-3p promoted the proliferation, invasion and migration of OCI-AML2 cells, and induced the cell cycle arrest in G1/S phase as well as inhibited cell apoptosis. Further studies showed that MVs promoted the proliferation, migration and invasion of AML, and induced the cell cycle arrest in G1/S phase through miR-221-3p. It was confirmed that miR-221-3p can directly target CDKN1C to regulate cell cycle, proliferation and invasion of AML. Conclusion: miR-221-3p in BMMSC-derived MVs regulated AML cell cycle, cell proliferation and invasion through targeting CDKN1C. miR-221-3p and CDKN1C were considered to be potential targets and biomarkers for the treatment of AML in clinic. Frontiers Media S.A. 2020-02-14 /pmc/articles/PMC7033425/ /pubmed/32117949 http://dx.doi.org/10.3389/fbioe.2020.00081 Text en Copyright © 2020 Zhang, Xu, Wang, Zhao, Li, Huang, Xu, Zhang, Suo, Lv, Zhang and Yu. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Bioengineering and Biotechnology
Zhang, Xuewu
Xu, Yu
Wang, Jinghan
Zhao, Shuqi
Li, Jianhu
Huang, Xin
Xu, Huan
Zhang, Xiang
Suo, Shanshan
Lv, Yunfei
Zhang, Yi
Yu, Wenjuan
miR-221-3p Delivered by BMMSC-Derived Microvesicles Promotes the Development of Acute Myelocytic Leukemia
title miR-221-3p Delivered by BMMSC-Derived Microvesicles Promotes the Development of Acute Myelocytic Leukemia
title_full miR-221-3p Delivered by BMMSC-Derived Microvesicles Promotes the Development of Acute Myelocytic Leukemia
title_fullStr miR-221-3p Delivered by BMMSC-Derived Microvesicles Promotes the Development of Acute Myelocytic Leukemia
title_full_unstemmed miR-221-3p Delivered by BMMSC-Derived Microvesicles Promotes the Development of Acute Myelocytic Leukemia
title_short miR-221-3p Delivered by BMMSC-Derived Microvesicles Promotes the Development of Acute Myelocytic Leukemia
title_sort mir-221-3p delivered by bmmsc-derived microvesicles promotes the development of acute myelocytic leukemia
topic Bioengineering and Biotechnology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7033425/
https://www.ncbi.nlm.nih.gov/pubmed/32117949
http://dx.doi.org/10.3389/fbioe.2020.00081
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