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LncRNA UCA1 promotes tumor metastasis by inducing miR-203/ZEB2 axis in gastric cancer
Increasing studies showed that long-noncoding RNAs (lncRNAs) play important roles in the biological processes, including cancer initiation and progression. However, little is known about the exact role and regulation mechanism of lncRNA UCA1 during the progression of gastric cancer (GC). In this stu...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6249325/ https://www.ncbi.nlm.nih.gov/pubmed/30464170 http://dx.doi.org/10.1038/s41419-018-1170-0 |
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author | Gong, Pihai Qiao, Fengchang Wu, Huazhang Cui, He Li, Yiping Zheng, Ying Zhou, Menghan Fan, Hong |
author_facet | Gong, Pihai Qiao, Fengchang Wu, Huazhang Cui, He Li, Yiping Zheng, Ying Zhou, Menghan Fan, Hong |
author_sort | Gong, Pihai |
collection | PubMed |
description | Increasing studies showed that long-noncoding RNAs (lncRNAs) play important roles in the biological processes, including cancer initiation and progression. However, little is known about the exact role and regulation mechanism of lncRNA UCA1 during the progression of gastric cancer (GC). In this study, we found that UCA1 was aberrantly elevated in gastric cancer tissues, and was significantly associated with lymph node metastasis and TNM stage. In vivo and in vitro, enforced UCA1 level promoted cell migration and invasion of GC cell. Depleted UCA1 expression level attenuated the ability of cell migration and invasion in GC. And then, we detected that expression level of ZEB2, a transcription factor related to tumor metastasis, was regulated by UCA1 in GC cells. miR-203 targets and suppresses to ZEB2 expression. Furthermore, we found that UCA1 could directly interact with miR-203 and lead to the release of miR-203-targeted transcripts ZEB2. Herein, we revealed the novel mechanism of UCA1 on regulating metastasis-related gene by sponge regulatory axis during GC metastasis. Our findings indicated that UCA1 plays a critical role in metastatic GC by mediating sponge regulatory axis miR-203/ZEB2. To explore function of UCA1-miR-203-ZEB2 axis may provide an informative biomarker of malignancy and a highly selective anti-GC therapeutic target. |
format | Online Article Text |
id | pubmed-6249325 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-62493252018-11-26 LncRNA UCA1 promotes tumor metastasis by inducing miR-203/ZEB2 axis in gastric cancer Gong, Pihai Qiao, Fengchang Wu, Huazhang Cui, He Li, Yiping Zheng, Ying Zhou, Menghan Fan, Hong Cell Death Dis Article Increasing studies showed that long-noncoding RNAs (lncRNAs) play important roles in the biological processes, including cancer initiation and progression. However, little is known about the exact role and regulation mechanism of lncRNA UCA1 during the progression of gastric cancer (GC). In this study, we found that UCA1 was aberrantly elevated in gastric cancer tissues, and was significantly associated with lymph node metastasis and TNM stage. In vivo and in vitro, enforced UCA1 level promoted cell migration and invasion of GC cell. Depleted UCA1 expression level attenuated the ability of cell migration and invasion in GC. And then, we detected that expression level of ZEB2, a transcription factor related to tumor metastasis, was regulated by UCA1 in GC cells. miR-203 targets and suppresses to ZEB2 expression. Furthermore, we found that UCA1 could directly interact with miR-203 and lead to the release of miR-203-targeted transcripts ZEB2. Herein, we revealed the novel mechanism of UCA1 on regulating metastasis-related gene by sponge regulatory axis during GC metastasis. Our findings indicated that UCA1 plays a critical role in metastatic GC by mediating sponge regulatory axis miR-203/ZEB2. To explore function of UCA1-miR-203-ZEB2 axis may provide an informative biomarker of malignancy and a highly selective anti-GC therapeutic target. Nature Publishing Group UK 2018-11-21 /pmc/articles/PMC6249325/ /pubmed/30464170 http://dx.doi.org/10.1038/s41419-018-1170-0 Text en © The Author(s) 2018 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 Gong, Pihai Qiao, Fengchang Wu, Huazhang Cui, He Li, Yiping Zheng, Ying Zhou, Menghan Fan, Hong LncRNA UCA1 promotes tumor metastasis by inducing miR-203/ZEB2 axis in gastric cancer |
title | LncRNA UCA1 promotes tumor metastasis by inducing miR-203/ZEB2 axis in gastric cancer |
title_full | LncRNA UCA1 promotes tumor metastasis by inducing miR-203/ZEB2 axis in gastric cancer |
title_fullStr | LncRNA UCA1 promotes tumor metastasis by inducing miR-203/ZEB2 axis in gastric cancer |
title_full_unstemmed | LncRNA UCA1 promotes tumor metastasis by inducing miR-203/ZEB2 axis in gastric cancer |
title_short | LncRNA UCA1 promotes tumor metastasis by inducing miR-203/ZEB2 axis in gastric cancer |
title_sort | lncrna uca1 promotes tumor metastasis by inducing mir-203/zeb2 axis in gastric cancer |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6249325/ https://www.ncbi.nlm.nih.gov/pubmed/30464170 http://dx.doi.org/10.1038/s41419-018-1170-0 |
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