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Silencing of MALAT1 inhibits migration and invasion by sponging miR-1-3p in prostate cancer cells
Prostate cancer is a common malignancy with a high mortality rate. Long non-coding RNA metastasis associated with lung adenocarcinoma transcript 1 (MALAT1) has been reported to serve tumor-promoting roles. However, the underlying mechanism requires further examination. In the present study, it was d...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6755148/ https://www.ncbi.nlm.nih.gov/pubmed/31485645 http://dx.doi.org/10.3892/mmr.2019.10602 |
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author | Dai, Xiaofan Liang, Zuowen Liu, Lingyun Guo, Kaimin Xu, Shengqi Wang, Hongliang |
author_facet | Dai, Xiaofan Liang, Zuowen Liu, Lingyun Guo, Kaimin Xu, Shengqi Wang, Hongliang |
author_sort | Dai, Xiaofan |
collection | PubMed |
description | Prostate cancer is a common malignancy with a high mortality rate. Long non-coding RNA metastasis associated with lung adenocarcinoma transcript 1 (MALAT1) has been reported to serve tumor-promoting roles. However, the underlying mechanism requires further examination. In the present study, it was demonstrated that MALAT1 was increased while microRNA (miR/miRNA)-1-3p was decreased in prostate cancer cell lines. The silencing of MALAT1 inhibited migration, invasion and epithelial-mesenchymal transition, when epithelial (E)-cadherin expression level was increased, and neural (N)-cadherin, vimentin, Slug and Snail expression levels were decreased. Dual-luciferase reporter assay results demonstrated that miR-1-3p bound to MALAT1 and coronin 1C (CORO1C) 3′ untranslated region, and MALAT1 competed with CORO1C for the binding sites of miR-1-3p. MALAT1 inhibited the expression of miR-1-3p and vice versa. MALAT1 knockdown induced the decline of CORO1C, which was subsequently recovered by the miR-1-3p inhibitor. In addition, by inhibiting miR-1-3p or overexpressing CORO1C, the silencing of MALAT1-induced phenotypic alterations were restored. In conclusion, MALAT1 serving as a degradable miRNA sponge, may sequester miR-1-3p from CORO1C and by silencing MALAT1, migration, invasion and epithelial-mesenchymal transition may be inhibited in prostate cancer cells. MALAT1 and CORO1C may serve as novel clinical therapeutic targets for prostate cancer. |
format | Online Article Text |
id | pubmed-6755148 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-67551482019-09-25 Silencing of MALAT1 inhibits migration and invasion by sponging miR-1-3p in prostate cancer cells Dai, Xiaofan Liang, Zuowen Liu, Lingyun Guo, Kaimin Xu, Shengqi Wang, Hongliang Mol Med Rep Articles Prostate cancer is a common malignancy with a high mortality rate. Long non-coding RNA metastasis associated with lung adenocarcinoma transcript 1 (MALAT1) has been reported to serve tumor-promoting roles. However, the underlying mechanism requires further examination. In the present study, it was demonstrated that MALAT1 was increased while microRNA (miR/miRNA)-1-3p was decreased in prostate cancer cell lines. The silencing of MALAT1 inhibited migration, invasion and epithelial-mesenchymal transition, when epithelial (E)-cadherin expression level was increased, and neural (N)-cadherin, vimentin, Slug and Snail expression levels were decreased. Dual-luciferase reporter assay results demonstrated that miR-1-3p bound to MALAT1 and coronin 1C (CORO1C) 3′ untranslated region, and MALAT1 competed with CORO1C for the binding sites of miR-1-3p. MALAT1 inhibited the expression of miR-1-3p and vice versa. MALAT1 knockdown induced the decline of CORO1C, which was subsequently recovered by the miR-1-3p inhibitor. In addition, by inhibiting miR-1-3p or overexpressing CORO1C, the silencing of MALAT1-induced phenotypic alterations were restored. In conclusion, MALAT1 serving as a degradable miRNA sponge, may sequester miR-1-3p from CORO1C and by silencing MALAT1, migration, invasion and epithelial-mesenchymal transition may be inhibited in prostate cancer cells. MALAT1 and CORO1C may serve as novel clinical therapeutic targets for prostate cancer. D.A. Spandidos 2019-10 2019-08-22 /pmc/articles/PMC6755148/ /pubmed/31485645 http://dx.doi.org/10.3892/mmr.2019.10602 Text en Copyright: © Dai et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , 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 | Articles Dai, Xiaofan Liang, Zuowen Liu, Lingyun Guo, Kaimin Xu, Shengqi Wang, Hongliang Silencing of MALAT1 inhibits migration and invasion by sponging miR-1-3p in prostate cancer cells |
title | Silencing of MALAT1 inhibits migration and invasion by sponging miR-1-3p in prostate cancer cells |
title_full | Silencing of MALAT1 inhibits migration and invasion by sponging miR-1-3p in prostate cancer cells |
title_fullStr | Silencing of MALAT1 inhibits migration and invasion by sponging miR-1-3p in prostate cancer cells |
title_full_unstemmed | Silencing of MALAT1 inhibits migration and invasion by sponging miR-1-3p in prostate cancer cells |
title_short | Silencing of MALAT1 inhibits migration and invasion by sponging miR-1-3p in prostate cancer cells |
title_sort | silencing of malat1 inhibits migration and invasion by sponging mir-1-3p in prostate cancer cells |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6755148/ https://www.ncbi.nlm.nih.gov/pubmed/31485645 http://dx.doi.org/10.3892/mmr.2019.10602 |
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