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CircME1 promotes aerobic glycolysis and sunitinib resistance of clear cell renal cell carcinoma through cis-regulation of ME1
Circular RNAs (circRNAs) play critical roles in clear cell renal cell carcinoma (ccRCC). However, their involvement in sunitinib resistance remains largely unknown. Herein, we identified a novel circRNA, named circME1, which contributes to sunitinib resistance development in ccRCC. CircME1 also prom...
Autores principales: | , , , , , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Nature Publishing Group UK
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9374592/ https://www.ncbi.nlm.nih.gov/pubmed/35798876 http://dx.doi.org/10.1038/s41388-022-02386-8 |
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author | Zhang, Ming-xiao Wang, Jia-li Mo, Cheng-qiang Mao, Xiao-peng Feng, Zi-hao Li, Jia-ying Lin, Hai-shan Song, Hong-de Xu, Quan-hui Wang, Ying-han Lu, Jun Wei, Jin-huan Han, Hui Chen, Wei Mao, Hai-ping Luo, Jun-hang Chen, Zhen-hua |
author_facet | Zhang, Ming-xiao Wang, Jia-li Mo, Cheng-qiang Mao, Xiao-peng Feng, Zi-hao Li, Jia-ying Lin, Hai-shan Song, Hong-de Xu, Quan-hui Wang, Ying-han Lu, Jun Wei, Jin-huan Han, Hui Chen, Wei Mao, Hai-ping Luo, Jun-hang Chen, Zhen-hua |
author_sort | Zhang, Ming-xiao |
collection | PubMed |
description | Circular RNAs (circRNAs) play critical roles in clear cell renal cell carcinoma (ccRCC). However, their involvement in sunitinib resistance remains largely unknown. Herein, we identified a novel circRNA, named circME1, which contributes to sunitinib resistance development in ccRCC. CircME1 also promoted proliferation, migration, and invasion of ccRCC cells. Further mechanism analysis showed that circME1 interacted with U1 snRNP at the promoter of its parental gene ME1, thereby upregulating the expression of ME1, enhancing aerobic glycolysis of ccRCC, and promoting its malignant phenotype. Furthermore, ME1 specific inhibitor could effectively repress the oncogenic functions of circME1. Taken together, our study demonstrates that the circME1/ME1 pathway is involved in ccRCC progression and sunitinib resistance development, which may be exploited for anticancer therapy. |
format | Online Article Text |
id | pubmed-9374592 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-93745922022-08-14 CircME1 promotes aerobic glycolysis and sunitinib resistance of clear cell renal cell carcinoma through cis-regulation of ME1 Zhang, Ming-xiao Wang, Jia-li Mo, Cheng-qiang Mao, Xiao-peng Feng, Zi-hao Li, Jia-ying Lin, Hai-shan Song, Hong-de Xu, Quan-hui Wang, Ying-han Lu, Jun Wei, Jin-huan Han, Hui Chen, Wei Mao, Hai-ping Luo, Jun-hang Chen, Zhen-hua Oncogene Article Circular RNAs (circRNAs) play critical roles in clear cell renal cell carcinoma (ccRCC). However, their involvement in sunitinib resistance remains largely unknown. Herein, we identified a novel circRNA, named circME1, which contributes to sunitinib resistance development in ccRCC. CircME1 also promoted proliferation, migration, and invasion of ccRCC cells. Further mechanism analysis showed that circME1 interacted with U1 snRNP at the promoter of its parental gene ME1, thereby upregulating the expression of ME1, enhancing aerobic glycolysis of ccRCC, and promoting its malignant phenotype. Furthermore, ME1 specific inhibitor could effectively repress the oncogenic functions of circME1. Taken together, our study demonstrates that the circME1/ME1 pathway is involved in ccRCC progression and sunitinib resistance development, which may be exploited for anticancer therapy. Nature Publishing Group UK 2022-07-07 2022 /pmc/articles/PMC9374592/ /pubmed/35798876 http://dx.doi.org/10.1038/s41388-022-02386-8 Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Article Zhang, Ming-xiao Wang, Jia-li Mo, Cheng-qiang Mao, Xiao-peng Feng, Zi-hao Li, Jia-ying Lin, Hai-shan Song, Hong-de Xu, Quan-hui Wang, Ying-han Lu, Jun Wei, Jin-huan Han, Hui Chen, Wei Mao, Hai-ping Luo, Jun-hang Chen, Zhen-hua CircME1 promotes aerobic glycolysis and sunitinib resistance of clear cell renal cell carcinoma through cis-regulation of ME1 |
title | CircME1 promotes aerobic glycolysis and sunitinib resistance of clear cell renal cell carcinoma through cis-regulation of ME1 |
title_full | CircME1 promotes aerobic glycolysis and sunitinib resistance of clear cell renal cell carcinoma through cis-regulation of ME1 |
title_fullStr | CircME1 promotes aerobic glycolysis and sunitinib resistance of clear cell renal cell carcinoma through cis-regulation of ME1 |
title_full_unstemmed | CircME1 promotes aerobic glycolysis and sunitinib resistance of clear cell renal cell carcinoma through cis-regulation of ME1 |
title_short | CircME1 promotes aerobic glycolysis and sunitinib resistance of clear cell renal cell carcinoma through cis-regulation of ME1 |
title_sort | circme1 promotes aerobic glycolysis and sunitinib resistance of clear cell renal cell carcinoma through cis-regulation of me1 |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9374592/ https://www.ncbi.nlm.nih.gov/pubmed/35798876 http://dx.doi.org/10.1038/s41388-022-02386-8 |
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