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DGUOK-AS1 acts as a tumorpromoter through regulatingmiR-204-5p/IL-11 axis in breast cancer
Breast cancer is one of the most lethal malignancies among women; however, the underlying molecular mechanism involved in the progression and metastasis of breast cancer remains unclear. Numerous studies have confirmed that long noncoding RNAs are abnormally expressed in breast cancer and play cruci...
Autores principales: | , , , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
American Society of Gene & Cell Therapy
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8571540/ https://www.ncbi.nlm.nih.gov/pubmed/34786212 http://dx.doi.org/10.1016/j.omtn.2021.10.018 |
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author | Liang, Yiran Ye, Fangzhou Wang, Yajie Li, Yalun Li, Yaming Song, Xiaojin Luo, Dan Long, Li Han, Dianwen Liu, Ying Wang, Zekun Chen, Bing Zhao, Wenjing Wang, Lijuan Yang, Qifeng |
author_facet | Liang, Yiran Ye, Fangzhou Wang, Yajie Li, Yalun Li, Yaming Song, Xiaojin Luo, Dan Long, Li Han, Dianwen Liu, Ying Wang, Zekun Chen, Bing Zhao, Wenjing Wang, Lijuan Yang, Qifeng |
author_sort | Liang, Yiran |
collection | PubMed |
description | Breast cancer is one of the most lethal malignancies among women; however, the underlying molecular mechanism involved in the progression and metastasis of breast cancer remains unclear. Numerous studies have confirmed that long noncoding RNAs are abnormally expressed in breast cancer and play crucial roles in cell proliferation and metastasis. In the study, we evaluated the functional role and detailed mechanism of DGUOK-AS1 in breast cancer progression and metastasis. DGUOK-AS1 knockdown suppressed proliferation, migration, and invasion of breast cancer cells in vitro and in vivo. Mechanistically, miR-204-5p was identified as an inhibitory target of DGUOK-AS1, which served as a tumor suppressor in breast cancer. Significantly, we found that the ectopic expression of miR-204-5p could counteract DGUOK-AS1-mediated promotion of cell proliferation and metastasis in breast cancer. Moreover, IL-11 was found to be the downstream target of miR-204-5p, and DGUOK-AS1 could protect IL-11 from miR-204-5p-mediated degradation. DGUOK-AS1 overexpression promoted breast cancer cell migration, angiogenesis, and macrophage migration, mediating by the increased secretion of IL-11, which was extremely important for cancer progression. Collectively, our studies reveal that DGUOK-AS1/miR-204-5p/IL-11 axis plays a significant role in the progression and metastasis of breast cancer, and DGUOK-AS1 might be a novel biomarker and therapeutic target for breast cancer. |
format | Online Article Text |
id | pubmed-8571540 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | American Society of Gene & Cell Therapy |
record_format | MEDLINE/PubMed |
spelling | pubmed-85715402021-11-15 DGUOK-AS1 acts as a tumorpromoter through regulatingmiR-204-5p/IL-11 axis in breast cancer Liang, Yiran Ye, Fangzhou Wang, Yajie Li, Yalun Li, Yaming Song, Xiaojin Luo, Dan Long, Li Han, Dianwen Liu, Ying Wang, Zekun Chen, Bing Zhao, Wenjing Wang, Lijuan Yang, Qifeng Mol Ther Nucleic Acids Original Article Breast cancer is one of the most lethal malignancies among women; however, the underlying molecular mechanism involved in the progression and metastasis of breast cancer remains unclear. Numerous studies have confirmed that long noncoding RNAs are abnormally expressed in breast cancer and play crucial roles in cell proliferation and metastasis. In the study, we evaluated the functional role and detailed mechanism of DGUOK-AS1 in breast cancer progression and metastasis. DGUOK-AS1 knockdown suppressed proliferation, migration, and invasion of breast cancer cells in vitro and in vivo. Mechanistically, miR-204-5p was identified as an inhibitory target of DGUOK-AS1, which served as a tumor suppressor in breast cancer. Significantly, we found that the ectopic expression of miR-204-5p could counteract DGUOK-AS1-mediated promotion of cell proliferation and metastasis in breast cancer. Moreover, IL-11 was found to be the downstream target of miR-204-5p, and DGUOK-AS1 could protect IL-11 from miR-204-5p-mediated degradation. DGUOK-AS1 overexpression promoted breast cancer cell migration, angiogenesis, and macrophage migration, mediating by the increased secretion of IL-11, which was extremely important for cancer progression. Collectively, our studies reveal that DGUOK-AS1/miR-204-5p/IL-11 axis plays a significant role in the progression and metastasis of breast cancer, and DGUOK-AS1 might be a novel biomarker and therapeutic target for breast cancer. American Society of Gene & Cell Therapy 2021-10-19 /pmc/articles/PMC8571540/ /pubmed/34786212 http://dx.doi.org/10.1016/j.omtn.2021.10.018 Text en © 2021 The Author(s) https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/). |
spellingShingle | Original Article Liang, Yiran Ye, Fangzhou Wang, Yajie Li, Yalun Li, Yaming Song, Xiaojin Luo, Dan Long, Li Han, Dianwen Liu, Ying Wang, Zekun Chen, Bing Zhao, Wenjing Wang, Lijuan Yang, Qifeng DGUOK-AS1 acts as a tumorpromoter through regulatingmiR-204-5p/IL-11 axis in breast cancer |
title | DGUOK-AS1 acts as a tumorpromoter through regulatingmiR-204-5p/IL-11 axis in breast cancer |
title_full | DGUOK-AS1 acts as a tumorpromoter through regulatingmiR-204-5p/IL-11 axis in breast cancer |
title_fullStr | DGUOK-AS1 acts as a tumorpromoter through regulatingmiR-204-5p/IL-11 axis in breast cancer |
title_full_unstemmed | DGUOK-AS1 acts as a tumorpromoter through regulatingmiR-204-5p/IL-11 axis in breast cancer |
title_short | DGUOK-AS1 acts as a tumorpromoter through regulatingmiR-204-5p/IL-11 axis in breast cancer |
title_sort | dguok-as1 acts as a tumorpromoter through regulatingmir-204-5p/il-11 axis in breast cancer |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8571540/ https://www.ncbi.nlm.nih.gov/pubmed/34786212 http://dx.doi.org/10.1016/j.omtn.2021.10.018 |
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