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Interference of the long noncoding RNA CDKN2B‐AS1 upregulates miR‐181a‐5p/TGFβI axis to restrain the metastasis and promote apoptosis and senescence of cervical cancer cells
Long noncoding RNA (lncRNA) CDKN2B‐AS1 has been shown to play a crucial role in the development as well as in the prognosis of various human cancers, including cervical cancer. However, the underlying mechanisms need to be further explored between CDKN2B‐AS1 and cervical cancer. In the present study...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6488111/ https://www.ncbi.nlm.nih.gov/pubmed/30884187 http://dx.doi.org/10.1002/cam4.2040 |
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author | Zhu, Lihong Zhang, Quanhua Li, Shaoping Jiang, Shan Cui, Jingjing Dang, Ge |
author_facet | Zhu, Lihong Zhang, Quanhua Li, Shaoping Jiang, Shan Cui, Jingjing Dang, Ge |
author_sort | Zhu, Lihong |
collection | PubMed |
description | Long noncoding RNA (lncRNA) CDKN2B‐AS1 has been shown to play a crucial role in the development as well as in the prognosis of various human cancers, including cervical cancer. However, the underlying mechanisms need to be further explored between CDKN2B‐AS1 and cervical cancer. In the present study, RT‐PCR showed that the mRNA level of CDKN2B‐AS1 was significantly upregulated while the miR‐181a‐5p was downregulated in cervical cancer cell lines. In addition, the interference of CDKN2B‐AS1 by shRNA resulted in the suppression of cell proliferation, invasion, migration and promotion of apoptosis and senescence, and either CDKN2B‐AS1 overexpression or miR‐181a‐5p showed reversed results. Further studies demonstrated that CDKN2B‐AS1 could directly interact with miR‐181a‐5p, and that there was an inverse correlation between miR‐181a‐5p and CDKN2B‐AS1. In addition, we found that TGFβI was a target of miR‐181a‐5p and could be downregulated by CDKN2B‐AS1 knockdown. Moreover, the in vivo experiments further demonstrated the contribution of CDKN2B‐AS1 in cervical cancer including tumor growth, apoptosis inhibition and senescence inhibition, and CDKN2B‐AS1 knockdown could inhibit the aforementioned activities. In summary, our study demonstrated that the CDKN2B‐AS1/miR‐181a‐5p/TGFβI axis might play a vital role in cervical cancer development. |
format | Online Article Text |
id | pubmed-6488111 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-64881112019-05-23 Interference of the long noncoding RNA CDKN2B‐AS1 upregulates miR‐181a‐5p/TGFβI axis to restrain the metastasis and promote apoptosis and senescence of cervical cancer cells Zhu, Lihong Zhang, Quanhua Li, Shaoping Jiang, Shan Cui, Jingjing Dang, Ge Cancer Med Cancer Biology Long noncoding RNA (lncRNA) CDKN2B‐AS1 has been shown to play a crucial role in the development as well as in the prognosis of various human cancers, including cervical cancer. However, the underlying mechanisms need to be further explored between CDKN2B‐AS1 and cervical cancer. In the present study, RT‐PCR showed that the mRNA level of CDKN2B‐AS1 was significantly upregulated while the miR‐181a‐5p was downregulated in cervical cancer cell lines. In addition, the interference of CDKN2B‐AS1 by shRNA resulted in the suppression of cell proliferation, invasion, migration and promotion of apoptosis and senescence, and either CDKN2B‐AS1 overexpression or miR‐181a‐5p showed reversed results. Further studies demonstrated that CDKN2B‐AS1 could directly interact with miR‐181a‐5p, and that there was an inverse correlation between miR‐181a‐5p and CDKN2B‐AS1. In addition, we found that TGFβI was a target of miR‐181a‐5p and could be downregulated by CDKN2B‐AS1 knockdown. Moreover, the in vivo experiments further demonstrated the contribution of CDKN2B‐AS1 in cervical cancer including tumor growth, apoptosis inhibition and senescence inhibition, and CDKN2B‐AS1 knockdown could inhibit the aforementioned activities. In summary, our study demonstrated that the CDKN2B‐AS1/miR‐181a‐5p/TGFβI axis might play a vital role in cervical cancer development. John Wiley and Sons Inc. 2019-03-18 /pmc/articles/PMC6488111/ /pubmed/30884187 http://dx.doi.org/10.1002/cam4.2040 Text en © 2019 The Authors. Cancer Medicine published by John Wiley & Sons Ltd. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Cancer Biology Zhu, Lihong Zhang, Quanhua Li, Shaoping Jiang, Shan Cui, Jingjing Dang, Ge Interference of the long noncoding RNA CDKN2B‐AS1 upregulates miR‐181a‐5p/TGFβI axis to restrain the metastasis and promote apoptosis and senescence of cervical cancer cells |
title | Interference of the long noncoding RNA CDKN2B‐AS1 upregulates miR‐181a‐5p/TGFβI axis to restrain the metastasis and promote apoptosis and senescence of cervical cancer cells |
title_full | Interference of the long noncoding RNA CDKN2B‐AS1 upregulates miR‐181a‐5p/TGFβI axis to restrain the metastasis and promote apoptosis and senescence of cervical cancer cells |
title_fullStr | Interference of the long noncoding RNA CDKN2B‐AS1 upregulates miR‐181a‐5p/TGFβI axis to restrain the metastasis and promote apoptosis and senescence of cervical cancer cells |
title_full_unstemmed | Interference of the long noncoding RNA CDKN2B‐AS1 upregulates miR‐181a‐5p/TGFβI axis to restrain the metastasis and promote apoptosis and senescence of cervical cancer cells |
title_short | Interference of the long noncoding RNA CDKN2B‐AS1 upregulates miR‐181a‐5p/TGFβI axis to restrain the metastasis and promote apoptosis and senescence of cervical cancer cells |
title_sort | interference of the long noncoding rna cdkn2b‐as1 upregulates mir‐181a‐5p/tgfβi axis to restrain the metastasis and promote apoptosis and senescence of cervical cancer cells |
topic | Cancer Biology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6488111/ https://www.ncbi.nlm.nih.gov/pubmed/30884187 http://dx.doi.org/10.1002/cam4.2040 |
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