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The YY1/miR-548t-5p/CXCL11 signaling axis regulates cell proliferation and metastasis in human pancreatic cancer
Pancreatic cancer (PC) is a malignant tumor with a poor prognosis and high mortality. However, the biological role of miR-548t-5p in PC has not been reported. In this study, we found that miR-548t-5p expression was significantly decreased in PC tissues compared with adjacent tissues, and that low mi...
Autores principales: | , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7186231/ https://www.ncbi.nlm.nih.gov/pubmed/32341359 http://dx.doi.org/10.1038/s41419-020-2475-3 |
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author | Ge, Wan-Li Chen, Qun Meng, Ling-Dong Huang, Xu-Min Shi, Guo-dong Zong, Qing-Qing Shen, Peng Lu, Yi-Chao Zhang, Yi-Han Miao, Yi Zhang, Jing-Jing Jiang, Kui-Rong |
author_facet | Ge, Wan-Li Chen, Qun Meng, Ling-Dong Huang, Xu-Min Shi, Guo-dong Zong, Qing-Qing Shen, Peng Lu, Yi-Chao Zhang, Yi-Han Miao, Yi Zhang, Jing-Jing Jiang, Kui-Rong |
author_sort | Ge, Wan-Li |
collection | PubMed |
description | Pancreatic cancer (PC) is a malignant tumor with a poor prognosis and high mortality. However, the biological role of miR-548t-5p in PC has not been reported. In this study, we found that miR-548t-5p expression was significantly decreased in PC tissues compared with adjacent tissues, and that low miR-548t-5p expression was associated with malignant PC behavior. In addition, high miR-548t-5p expression inhibited the proliferation, migration, and invasion of PC cell lines. Regarding the molecular mechanism, the luciferase reporter gene, chromatin immunoprecipitation (ChIP), and functional recovery assays revealed that YY1 binds to the miR-548t-5p promoter and positively regulates the expression and function of miR-548t-5p. miR-548t-5p also directly regulates CXCL11 to inhibit its expression. A high level of CXCL11 was associated with worse Tumor Node Metastasis (TNM) staging in patients with PC, enhancing proliferation and metastasis in PC cells. Our study shows that the YY1/miR-548t-5p/CXCL11 axis plays an important role in PC and provides a new potential candidate for the treatment of PC. |
format | Online Article Text |
id | pubmed-7186231 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-71862312020-04-30 The YY1/miR-548t-5p/CXCL11 signaling axis regulates cell proliferation and metastasis in human pancreatic cancer Ge, Wan-Li Chen, Qun Meng, Ling-Dong Huang, Xu-Min Shi, Guo-dong Zong, Qing-Qing Shen, Peng Lu, Yi-Chao Zhang, Yi-Han Miao, Yi Zhang, Jing-Jing Jiang, Kui-Rong Cell Death Dis Article Pancreatic cancer (PC) is a malignant tumor with a poor prognosis and high mortality. However, the biological role of miR-548t-5p in PC has not been reported. In this study, we found that miR-548t-5p expression was significantly decreased in PC tissues compared with adjacent tissues, and that low miR-548t-5p expression was associated with malignant PC behavior. In addition, high miR-548t-5p expression inhibited the proliferation, migration, and invasion of PC cell lines. Regarding the molecular mechanism, the luciferase reporter gene, chromatin immunoprecipitation (ChIP), and functional recovery assays revealed that YY1 binds to the miR-548t-5p promoter and positively regulates the expression and function of miR-548t-5p. miR-548t-5p also directly regulates CXCL11 to inhibit its expression. A high level of CXCL11 was associated with worse Tumor Node Metastasis (TNM) staging in patients with PC, enhancing proliferation and metastasis in PC cells. Our study shows that the YY1/miR-548t-5p/CXCL11 axis plays an important role in PC and provides a new potential candidate for the treatment of PC. Nature Publishing Group UK 2020-04-27 /pmc/articles/PMC7186231/ /pubmed/32341359 http://dx.doi.org/10.1038/s41419-020-2475-3 Text en © The Author(s) 2020 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/. |
spellingShingle | Article Ge, Wan-Li Chen, Qun Meng, Ling-Dong Huang, Xu-Min Shi, Guo-dong Zong, Qing-Qing Shen, Peng Lu, Yi-Chao Zhang, Yi-Han Miao, Yi Zhang, Jing-Jing Jiang, Kui-Rong The YY1/miR-548t-5p/CXCL11 signaling axis regulates cell proliferation and metastasis in human pancreatic cancer |
title | The YY1/miR-548t-5p/CXCL11 signaling axis regulates cell proliferation and metastasis in human pancreatic cancer |
title_full | The YY1/miR-548t-5p/CXCL11 signaling axis regulates cell proliferation and metastasis in human pancreatic cancer |
title_fullStr | The YY1/miR-548t-5p/CXCL11 signaling axis regulates cell proliferation and metastasis in human pancreatic cancer |
title_full_unstemmed | The YY1/miR-548t-5p/CXCL11 signaling axis regulates cell proliferation and metastasis in human pancreatic cancer |
title_short | The YY1/miR-548t-5p/CXCL11 signaling axis regulates cell proliferation and metastasis in human pancreatic cancer |
title_sort | yy1/mir-548t-5p/cxcl11 signaling axis regulates cell proliferation and metastasis in human pancreatic cancer |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7186231/ https://www.ncbi.nlm.nih.gov/pubmed/32341359 http://dx.doi.org/10.1038/s41419-020-2475-3 |
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