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Upregulation of exosomal circPLK1 promotes the development of non-small cell lung cancer through the miR-1294/ high mobility group protein A1 axis
CircRNAs (circular RNAs) have been implicated in the development and progression of a variety of cancers. The molecular pathways underlying the progression of NSCLC (Non-Small Cell Lung Cancer) and the associated regulation of circRNAs in NSCLC remain to be fully elucidated. In this study, we found...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Taylor & Francis
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8973815/ https://www.ncbi.nlm.nih.gov/pubmed/35114891 http://dx.doi.org/10.1080/21655979.2022.2026727 |
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author | Li, Chuankui Wang, Guowen Ma, Xiaoxiao Tao, Tao Li, Qicai Yang, Yifan Sang, Haiwei Wang, Zuyi |
author_facet | Li, Chuankui Wang, Guowen Ma, Xiaoxiao Tao, Tao Li, Qicai Yang, Yifan Sang, Haiwei Wang, Zuyi |
author_sort | Li, Chuankui |
collection | PubMed |
description | CircRNAs (circular RNAs) have been implicated in the development and progression of a variety of cancers. The molecular pathways underlying the progression of NSCLC (Non-Small Cell Lung Cancer) and the associated regulation of circRNAs in NSCLC remain to be fully elucidated. In this study, we found that circPLK1 expression was upregulated in serum exosomes and tissues from NSCLC patients. The Kaplan–Meier survival analysis revealed that a high expression level of circPLK1 was associated with a poorer prognosis in NSCLC patients. Exosomes extracted from NSCLC serum could promote the replication, migration, and invasion of NSCLC cells and suppress apoptotic cell death. The overexpression of circPLK1 also promotes the malignant phenotype of NSCLC cells. Molecular analyses demonstrated that circPLK1 directly targets miR-1294 and negatively regulates its activity. And circPLK1 overexpression facilitates the progression of NSCLC by negatively regulating miR-1294 level and maintaining a high-level expression of HMGA1 (High Mobility Group Protein A1). Our study suggests that circPLK1 upregulation plays an important role in NSCLC progression by targeting miR-1294/HMGA1 axis. These data provide a theoretical basis for the development of therapeutic strategy targeting exosomal circPLK1 in NSCLC treatment. |
format | Online Article Text |
id | pubmed-8973815 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Taylor & Francis |
record_format | MEDLINE/PubMed |
spelling | pubmed-89738152022-04-02 Upregulation of exosomal circPLK1 promotes the development of non-small cell lung cancer through the miR-1294/ high mobility group protein A1 axis Li, Chuankui Wang, Guowen Ma, Xiaoxiao Tao, Tao Li, Qicai Yang, Yifan Sang, Haiwei Wang, Zuyi Bioengineered Research Paper CircRNAs (circular RNAs) have been implicated in the development and progression of a variety of cancers. The molecular pathways underlying the progression of NSCLC (Non-Small Cell Lung Cancer) and the associated regulation of circRNAs in NSCLC remain to be fully elucidated. In this study, we found that circPLK1 expression was upregulated in serum exosomes and tissues from NSCLC patients. The Kaplan–Meier survival analysis revealed that a high expression level of circPLK1 was associated with a poorer prognosis in NSCLC patients. Exosomes extracted from NSCLC serum could promote the replication, migration, and invasion of NSCLC cells and suppress apoptotic cell death. The overexpression of circPLK1 also promotes the malignant phenotype of NSCLC cells. Molecular analyses demonstrated that circPLK1 directly targets miR-1294 and negatively regulates its activity. And circPLK1 overexpression facilitates the progression of NSCLC by negatively regulating miR-1294 level and maintaining a high-level expression of HMGA1 (High Mobility Group Protein A1). Our study suggests that circPLK1 upregulation plays an important role in NSCLC progression by targeting miR-1294/HMGA1 axis. These data provide a theoretical basis for the development of therapeutic strategy targeting exosomal circPLK1 in NSCLC treatment. Taylor & Francis 2022-02-03 /pmc/articles/PMC8973815/ /pubmed/35114891 http://dx.doi.org/10.1080/21655979.2022.2026727 Text en © 2022 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 Li, Chuankui Wang, Guowen Ma, Xiaoxiao Tao, Tao Li, Qicai Yang, Yifan Sang, Haiwei Wang, Zuyi Upregulation of exosomal circPLK1 promotes the development of non-small cell lung cancer through the miR-1294/ high mobility group protein A1 axis |
title | Upregulation of exosomal circPLK1 promotes the development of non-small cell lung cancer through the miR-1294/ high mobility group protein A1 axis |
title_full | Upregulation of exosomal circPLK1 promotes the development of non-small cell lung cancer through the miR-1294/ high mobility group protein A1 axis |
title_fullStr | Upregulation of exosomal circPLK1 promotes the development of non-small cell lung cancer through the miR-1294/ high mobility group protein A1 axis |
title_full_unstemmed | Upregulation of exosomal circPLK1 promotes the development of non-small cell lung cancer through the miR-1294/ high mobility group protein A1 axis |
title_short | Upregulation of exosomal circPLK1 promotes the development of non-small cell lung cancer through the miR-1294/ high mobility group protein A1 axis |
title_sort | upregulation of exosomal circplk1 promotes the development of non-small cell lung cancer through the mir-1294/ high mobility group protein a1 axis |
topic | Research Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8973815/ https://www.ncbi.nlm.nih.gov/pubmed/35114891 http://dx.doi.org/10.1080/21655979.2022.2026727 |
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