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A novel fusion circular RNA F-circBA1 derived from the BCR-ABL fusion gene displayed an oncogenic role in chronic myeloid leukemia cells
The BCR-ABL fusion gene plays a crucial role in the leukemogenesis of chronic myeloid leukemia (CML). The BCR-ABL oncoprotein encoded by this fusion gene has been extensively studied. However, research on whether BCR-ABL also affects circular RNAs (circRNAs) is limited. This study aimed to explore t...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Taylor & Francis
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8806869/ https://www.ncbi.nlm.nih.gov/pubmed/34346842 http://dx.doi.org/10.1080/21655979.2021.1957749 |
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author | Tan, Yuan Huang, Zhenglan Wang, Xin Dai, Hongdan Jiang, Guoyun Feng, Wenli |
author_facet | Tan, Yuan Huang, Zhenglan Wang, Xin Dai, Hongdan Jiang, Guoyun Feng, Wenli |
author_sort | Tan, Yuan |
collection | PubMed |
description | The BCR-ABL fusion gene plays a crucial role in the leukemogenesis of chronic myeloid leukemia (CML). The BCR-ABL oncoprotein encoded by this fusion gene has been extensively studied. However, research on whether BCR-ABL also affects circular RNAs (circRNAs) is limited. This study aimed to explore the new fusion circRNAs produced by BCR-ABL and their role in CML cells. In this study, we identified a novel fusion circRNA, named F-circBA1, originating from BCR-ABL in K562 and K562/G01 cells using quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR) and Sanger sequencing. qRT-PCR of the nuclear RNA and cytoplasmic RNA were separated, indicating that F-circBA1 was mainly localized in the cytoplasm. Cell counting kit-8 assay and flow cytometry showed that F-circBA1 knockdown by shRNA prevented the proliferation of K562 and K562/G01 cells, and the cell cycle was arrested at G2/M. Mechanically, dual-luciferase reporter assay and western blotting assay showed that F-circBA1 sponged miR-148-3p and F-circBA1 silencing decreased CDC25B expression in vitro. Furthermore, the results of the murine leukemogenesis model showed that F-circBA1 knockdown suppressed leukemogenesis in vivo. Besides, we found the existence of F-circBA1 in some patients with BCR-ABL-positive CML. In conclusion, these results demonstrate the presence of F-circBA1 and its oncogenic role in CML cells. |
format | Online Article Text |
id | pubmed-8806869 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Taylor & Francis |
record_format | MEDLINE/PubMed |
spelling | pubmed-88068692022-02-02 A novel fusion circular RNA F-circBA1 derived from the BCR-ABL fusion gene displayed an oncogenic role in chronic myeloid leukemia cells Tan, Yuan Huang, Zhenglan Wang, Xin Dai, Hongdan Jiang, Guoyun Feng, Wenli Bioengineered Research Paper The BCR-ABL fusion gene plays a crucial role in the leukemogenesis of chronic myeloid leukemia (CML). The BCR-ABL oncoprotein encoded by this fusion gene has been extensively studied. However, research on whether BCR-ABL also affects circular RNAs (circRNAs) is limited. This study aimed to explore the new fusion circRNAs produced by BCR-ABL and their role in CML cells. In this study, we identified a novel fusion circRNA, named F-circBA1, originating from BCR-ABL in K562 and K562/G01 cells using quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR) and Sanger sequencing. qRT-PCR of the nuclear RNA and cytoplasmic RNA were separated, indicating that F-circBA1 was mainly localized in the cytoplasm. Cell counting kit-8 assay and flow cytometry showed that F-circBA1 knockdown by shRNA prevented the proliferation of K562 and K562/G01 cells, and the cell cycle was arrested at G2/M. Mechanically, dual-luciferase reporter assay and western blotting assay showed that F-circBA1 sponged miR-148-3p and F-circBA1 silencing decreased CDC25B expression in vitro. Furthermore, the results of the murine leukemogenesis model showed that F-circBA1 knockdown suppressed leukemogenesis in vivo. Besides, we found the existence of F-circBA1 in some patients with BCR-ABL-positive CML. In conclusion, these results demonstrate the presence of F-circBA1 and its oncogenic role in CML cells. Taylor & Francis 2021-08-04 /pmc/articles/PMC8806869/ /pubmed/34346842 http://dx.doi.org/10.1080/21655979.2021.1957749 Text en © 2021 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. https://creativecommons.org/licenses/by/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Paper Tan, Yuan Huang, Zhenglan Wang, Xin Dai, Hongdan Jiang, Guoyun Feng, Wenli A novel fusion circular RNA F-circBA1 derived from the BCR-ABL fusion gene displayed an oncogenic role in chronic myeloid leukemia cells |
title | A novel fusion circular RNA F-circBA1 derived from the BCR-ABL fusion gene displayed an oncogenic role in chronic myeloid leukemia cells |
title_full | A novel fusion circular RNA F-circBA1 derived from the BCR-ABL fusion gene displayed an oncogenic role in chronic myeloid leukemia cells |
title_fullStr | A novel fusion circular RNA F-circBA1 derived from the BCR-ABL fusion gene displayed an oncogenic role in chronic myeloid leukemia cells |
title_full_unstemmed | A novel fusion circular RNA F-circBA1 derived from the BCR-ABL fusion gene displayed an oncogenic role in chronic myeloid leukemia cells |
title_short | A novel fusion circular RNA F-circBA1 derived from the BCR-ABL fusion gene displayed an oncogenic role in chronic myeloid leukemia cells |
title_sort | novel fusion circular rna f-circba1 derived from the bcr-abl fusion gene displayed an oncogenic role in chronic myeloid leukemia cells |
topic | Research Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8806869/ https://www.ncbi.nlm.nih.gov/pubmed/34346842 http://dx.doi.org/10.1080/21655979.2021.1957749 |
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