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CircCFL1/MiR-107 Axis Targeting HMGB1 Promotes the Malignant Progression of Diffuse Large B-Cell Lymphoma Tumors

OBJECTIVE: The pathogenesis of diffuse large B-cell lymphoma (DLBCL) has not yet been fully elucidated. An increasing number of studies have shown that circular RNAs (circRNAs) play an important role in tumorigenesis and development. The aim of this study was to investigate the effect of CircCFL1 on...

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Autores principales: Chen, Xiaowei, Xie, Xiaobin, Zhou, Wei
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7533230/
https://www.ncbi.nlm.nih.gov/pubmed/33061624
http://dx.doi.org/10.2147/CMAR.S263222
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author Chen, Xiaowei
Xie, Xiaobin
Zhou, Wei
author_facet Chen, Xiaowei
Xie, Xiaobin
Zhou, Wei
author_sort Chen, Xiaowei
collection PubMed
description OBJECTIVE: The pathogenesis of diffuse large B-cell lymphoma (DLBCL) has not yet been fully elucidated. An increasing number of studies have shown that circular RNAs (circRNAs) play an important role in tumorigenesis and development. The aim of this study was to investigate the effect of CircCFL1 on the malignant progression of DLBCL. METHODS: RT-qPCR was used to detect the expression levels of CircCFL1 and miR-107. A dual-luciferase reporter gene experiment was conducted to verify that CircCFL1 targeted miR-107 and the miR-107 target gene HMGB1. BrdU, transwell, and MTT tests were performed to detect cell invasion and proliferation. Western blot analysis was used to detect the phosphorylation of proteins. Xenograft models were established to confirm the effect of CircCFL1 on DLBCL tumor growth in vivo. RESULTS: The expression of CircCFL1 in cells transfected with the CircCFL1 overexpression vector was higher than that in the control group. After overexpressing CircCFL1, the expression of miR-107 in cells decreased significantly, and the protein level of HMGB1 increased. The dual-luciferase reporter gene experiment showed that CircCFL1 directly bound to miR-107 and reduced the inhibition of the target gene HMGB1. After CircCFL1 was overexpressed, cell migration and proliferation were enhanced. The tumor volume and weight in the lentivirus CircCFL1 group were higher than those in the lentivirus NC group. CONCLUSION: Results showed that the circRNA CircCFL1 could regulate the expression of HMGB1 through miR-107 to promote the proliferation and migration of DLBCL.
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spelling pubmed-75332302020-10-14 CircCFL1/MiR-107 Axis Targeting HMGB1 Promotes the Malignant Progression of Diffuse Large B-Cell Lymphoma Tumors Chen, Xiaowei Xie, Xiaobin Zhou, Wei Cancer Manag Res Original Research OBJECTIVE: The pathogenesis of diffuse large B-cell lymphoma (DLBCL) has not yet been fully elucidated. An increasing number of studies have shown that circular RNAs (circRNAs) play an important role in tumorigenesis and development. The aim of this study was to investigate the effect of CircCFL1 on the malignant progression of DLBCL. METHODS: RT-qPCR was used to detect the expression levels of CircCFL1 and miR-107. A dual-luciferase reporter gene experiment was conducted to verify that CircCFL1 targeted miR-107 and the miR-107 target gene HMGB1. BrdU, transwell, and MTT tests were performed to detect cell invasion and proliferation. Western blot analysis was used to detect the phosphorylation of proteins. Xenograft models were established to confirm the effect of CircCFL1 on DLBCL tumor growth in vivo. RESULTS: The expression of CircCFL1 in cells transfected with the CircCFL1 overexpression vector was higher than that in the control group. After overexpressing CircCFL1, the expression of miR-107 in cells decreased significantly, and the protein level of HMGB1 increased. The dual-luciferase reporter gene experiment showed that CircCFL1 directly bound to miR-107 and reduced the inhibition of the target gene HMGB1. After CircCFL1 was overexpressed, cell migration and proliferation were enhanced. The tumor volume and weight in the lentivirus CircCFL1 group were higher than those in the lentivirus NC group. CONCLUSION: Results showed that the circRNA CircCFL1 could regulate the expression of HMGB1 through miR-107 to promote the proliferation and migration of DLBCL. Dove 2020-09-30 /pmc/articles/PMC7533230/ /pubmed/33061624 http://dx.doi.org/10.2147/CMAR.S263222 Text en © 2020 Chen et al. http://creativecommons.org/licenses/by-nc/3.0/ This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php).
spellingShingle Original Research
Chen, Xiaowei
Xie, Xiaobin
Zhou, Wei
CircCFL1/MiR-107 Axis Targeting HMGB1 Promotes the Malignant Progression of Diffuse Large B-Cell Lymphoma Tumors
title CircCFL1/MiR-107 Axis Targeting HMGB1 Promotes the Malignant Progression of Diffuse Large B-Cell Lymphoma Tumors
title_full CircCFL1/MiR-107 Axis Targeting HMGB1 Promotes the Malignant Progression of Diffuse Large B-Cell Lymphoma Tumors
title_fullStr CircCFL1/MiR-107 Axis Targeting HMGB1 Promotes the Malignant Progression of Diffuse Large B-Cell Lymphoma Tumors
title_full_unstemmed CircCFL1/MiR-107 Axis Targeting HMGB1 Promotes the Malignant Progression of Diffuse Large B-Cell Lymphoma Tumors
title_short CircCFL1/MiR-107 Axis Targeting HMGB1 Promotes the Malignant Progression of Diffuse Large B-Cell Lymphoma Tumors
title_sort circcfl1/mir-107 axis targeting hmgb1 promotes the malignant progression of diffuse large b-cell lymphoma tumors
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7533230/
https://www.ncbi.nlm.nih.gov/pubmed/33061624
http://dx.doi.org/10.2147/CMAR.S263222
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