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Long noncoding RNA TP53TG1 promotes pancreatic ductal adenocarcinoma development by acting as a molecular sponge of microRNA‐96
Long noncoding RNAs (lncRNAs) are emerging as key regulators in cancer initiation and progression. TP53TG1 is a recently identified lncRNA and several studies have shown that TP53TG1 may play the role of tumor suppressor gene or oncogene in different tumors. Nevertheless, the involvement of TP53TG1...
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/PMC6726832/ https://www.ncbi.nlm.nih.gov/pubmed/31325400 http://dx.doi.org/10.1111/cas.14136 |
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author | Zhang, Yufeng Yang, Haiyan Du, Yong Liu, Pingping Zhang, Jing Li, Yue Shen, Haitao Xing, Lingxiao Xue, Xiaoying Chen, Jie Zhang, Xianghong |
author_facet | Zhang, Yufeng Yang, Haiyan Du, Yong Liu, Pingping Zhang, Jing Li, Yue Shen, Haitao Xing, Lingxiao Xue, Xiaoying Chen, Jie Zhang, Xianghong |
author_sort | Zhang, Yufeng |
collection | PubMed |
description | Long noncoding RNAs (lncRNAs) are emerging as key regulators in cancer initiation and progression. TP53TG1 is a recently identified lncRNA and several studies have shown that TP53TG1 may play the role of tumor suppressor gene or oncogene in different tumors. Nevertheless, the involvement of TP53TG1 in carcinogenesis of pancreatic ductal adenocarcinoma (PDAC) has not been characterized. In our studies, we identified that TP53TG1 was highly expressed in PDAC and was a novel regulator of PDAC development. Knockdown of TP53TG1 inhibited proliferation, induced apoptosis, and decreased migration and invasion in PDAC cells, whereas enhanced expression of TP53TG1 had the opposite effects. Mechanistically, TP53TG1 could directly bind to microRNA (miR)‐96 and effectively function as a sponge for miR‐96, thus antagonizing the functions of miR‐96 and leading to derepression of its endogenous target KRAS, which is a core oncogene in the initiation and maintenance of PDAC. Taken together, these observations imply that TP53TG1 contributes to the growth and progression of PDAC by acting as a competing endogenous RNA (ceRNA) to competitively bind to miR‐96 and regulate KRAS expression, which highlights the importance of the complicated miRNA‐lncRNA network in modulating the progression of PDAC. |
format | Online Article Text |
id | pubmed-6726832 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-67268322019-09-10 Long noncoding RNA TP53TG1 promotes pancreatic ductal adenocarcinoma development by acting as a molecular sponge of microRNA‐96 Zhang, Yufeng Yang, Haiyan Du, Yong Liu, Pingping Zhang, Jing Li, Yue Shen, Haitao Xing, Lingxiao Xue, Xiaoying Chen, Jie Zhang, Xianghong Cancer Sci Original Articles Long noncoding RNAs (lncRNAs) are emerging as key regulators in cancer initiation and progression. TP53TG1 is a recently identified lncRNA and several studies have shown that TP53TG1 may play the role of tumor suppressor gene or oncogene in different tumors. Nevertheless, the involvement of TP53TG1 in carcinogenesis of pancreatic ductal adenocarcinoma (PDAC) has not been characterized. In our studies, we identified that TP53TG1 was highly expressed in PDAC and was a novel regulator of PDAC development. Knockdown of TP53TG1 inhibited proliferation, induced apoptosis, and decreased migration and invasion in PDAC cells, whereas enhanced expression of TP53TG1 had the opposite effects. Mechanistically, TP53TG1 could directly bind to microRNA (miR)‐96 and effectively function as a sponge for miR‐96, thus antagonizing the functions of miR‐96 and leading to derepression of its endogenous target KRAS, which is a core oncogene in the initiation and maintenance of PDAC. Taken together, these observations imply that TP53TG1 contributes to the growth and progression of PDAC by acting as a competing endogenous RNA (ceRNA) to competitively bind to miR‐96 and regulate KRAS expression, which highlights the importance of the complicated miRNA‐lncRNA network in modulating the progression of PDAC. John Wiley and Sons Inc. 2019-08-07 2019-09 /pmc/articles/PMC6726832/ /pubmed/31325400 http://dx.doi.org/10.1111/cas.14136 Text en © 2019 The Authors. Cancer Science published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association. This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made. |
spellingShingle | Original Articles Zhang, Yufeng Yang, Haiyan Du, Yong Liu, Pingping Zhang, Jing Li, Yue Shen, Haitao Xing, Lingxiao Xue, Xiaoying Chen, Jie Zhang, Xianghong Long noncoding RNA TP53TG1 promotes pancreatic ductal adenocarcinoma development by acting as a molecular sponge of microRNA‐96 |
title | Long noncoding RNA TP53TG1 promotes pancreatic ductal adenocarcinoma development by acting as a molecular sponge of microRNA‐96 |
title_full | Long noncoding RNA TP53TG1 promotes pancreatic ductal adenocarcinoma development by acting as a molecular sponge of microRNA‐96 |
title_fullStr | Long noncoding RNA TP53TG1 promotes pancreatic ductal adenocarcinoma development by acting as a molecular sponge of microRNA‐96 |
title_full_unstemmed | Long noncoding RNA TP53TG1 promotes pancreatic ductal adenocarcinoma development by acting as a molecular sponge of microRNA‐96 |
title_short | Long noncoding RNA TP53TG1 promotes pancreatic ductal adenocarcinoma development by acting as a molecular sponge of microRNA‐96 |
title_sort | long noncoding rna tp53tg1 promotes pancreatic ductal adenocarcinoma development by acting as a molecular sponge of microrna‐96 |
topic | Original Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6726832/ https://www.ncbi.nlm.nih.gov/pubmed/31325400 http://dx.doi.org/10.1111/cas.14136 |
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