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Long non-coding RNA UCA1 promotes breast cancer by upregulating PTP1B expression via inhibiting miR-206
BACKGROUND: The long non-coding RNA (lncRNA) urothelial carcinoma-associated 1 (UCA1) is involved in various cancers and often functions through microRNAs. The pro-survival protein PTP1B is known to play important roles in cancer development. However, the connection between UCA1 and PTP1B in breast...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6824019/ https://www.ncbi.nlm.nih.gov/pubmed/31695578 http://dx.doi.org/10.1186/s12935-019-0958-z |
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author | Li, Yi Zeng, Qingan Qiu, Jiliang Pang, Ting Xian, Jianzhong Zhang, Xuexia |
author_facet | Li, Yi Zeng, Qingan Qiu, Jiliang Pang, Ting Xian, Jianzhong Zhang, Xuexia |
author_sort | Li, Yi |
collection | PubMed |
description | BACKGROUND: The long non-coding RNA (lncRNA) urothelial carcinoma-associated 1 (UCA1) is involved in various cancers and often functions through microRNAs. The pro-survival protein PTP1B is known to play important roles in cancer development. However, the connection between UCA1 and PTP1B in breast cancer is not well studied. METHODS: In this study, we first evaluated the correlation between UCA1 level and PTP1B expression in breast tissues, which showed the expression of PTP1B were much higher in the breast tumor tissues than in the peritumor normal tissues. The UCA1 level was positively associated with PTP1B expression in breast tumor tissues. RESULTS: We observed that UCA1 could up-regulate PTP1B expression in breast cancer cells. We also found that miR-206 could inhibit the expression of PTP1B by directly binding to the 3′-UTR of its mRNA. Interestingly, UCA1 could increase the expression of PTP1B through sequestering miR-206 at post-transcriptional level. The results also suggested that UCA1-induced PTP1B expression facilitated the proliferation of breast cancer cells. CONCLUSIONS: We conclude that UCA1 can up-regulates PTP1B to enhance cell proliferation through sequestering miR-206 in breast cancer. Our finding provides new insights into the mechanism of breast cancer regulation by UCA1, which could be a potential target for breast cancer treatment. Trial registration 2012N5hSYSU48573. Registered at Oct 12, 2012 |
format | Online Article Text |
id | pubmed-6824019 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-68240192019-11-06 Long non-coding RNA UCA1 promotes breast cancer by upregulating PTP1B expression via inhibiting miR-206 Li, Yi Zeng, Qingan Qiu, Jiliang Pang, Ting Xian, Jianzhong Zhang, Xuexia Cancer Cell Int Primary Research BACKGROUND: The long non-coding RNA (lncRNA) urothelial carcinoma-associated 1 (UCA1) is involved in various cancers and often functions through microRNAs. The pro-survival protein PTP1B is known to play important roles in cancer development. However, the connection between UCA1 and PTP1B in breast cancer is not well studied. METHODS: In this study, we first evaluated the correlation between UCA1 level and PTP1B expression in breast tissues, which showed the expression of PTP1B were much higher in the breast tumor tissues than in the peritumor normal tissues. The UCA1 level was positively associated with PTP1B expression in breast tumor tissues. RESULTS: We observed that UCA1 could up-regulate PTP1B expression in breast cancer cells. We also found that miR-206 could inhibit the expression of PTP1B by directly binding to the 3′-UTR of its mRNA. Interestingly, UCA1 could increase the expression of PTP1B through sequestering miR-206 at post-transcriptional level. The results also suggested that UCA1-induced PTP1B expression facilitated the proliferation of breast cancer cells. CONCLUSIONS: We conclude that UCA1 can up-regulates PTP1B to enhance cell proliferation through sequestering miR-206 in breast cancer. Our finding provides new insights into the mechanism of breast cancer regulation by UCA1, which could be a potential target for breast cancer treatment. Trial registration 2012N5hSYSU48573. Registered at Oct 12, 2012 BioMed Central 2019-11-01 /pmc/articles/PMC6824019/ /pubmed/31695578 http://dx.doi.org/10.1186/s12935-019-0958-z Text en © The Author(s) 2019 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
spellingShingle | Primary Research Li, Yi Zeng, Qingan Qiu, Jiliang Pang, Ting Xian, Jianzhong Zhang, Xuexia Long non-coding RNA UCA1 promotes breast cancer by upregulating PTP1B expression via inhibiting miR-206 |
title | Long non-coding RNA UCA1 promotes breast cancer by upregulating PTP1B expression via inhibiting miR-206 |
title_full | Long non-coding RNA UCA1 promotes breast cancer by upregulating PTP1B expression via inhibiting miR-206 |
title_fullStr | Long non-coding RNA UCA1 promotes breast cancer by upregulating PTP1B expression via inhibiting miR-206 |
title_full_unstemmed | Long non-coding RNA UCA1 promotes breast cancer by upregulating PTP1B expression via inhibiting miR-206 |
title_short | Long non-coding RNA UCA1 promotes breast cancer by upregulating PTP1B expression via inhibiting miR-206 |
title_sort | long non-coding rna uca1 promotes breast cancer by upregulating ptp1b expression via inhibiting mir-206 |
topic | Primary Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6824019/ https://www.ncbi.nlm.nih.gov/pubmed/31695578 http://dx.doi.org/10.1186/s12935-019-0958-z |
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