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MiR-384 inhibits the proliferation of colorectal cancer by targeting AKT3
BACKGROUND: Growing evidence suggests that MiRNAs play essential roles in the initiation and progression of colorectal cancer (CRC). The aberrant expression of miR-384 has been reported in some cancers. However, the role and mechanism of miR-384 in CRC proliferation remains unknown. METHODS: The exp...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6122463/ https://www.ncbi.nlm.nih.gov/pubmed/30186040 http://dx.doi.org/10.1186/s12935-018-0628-6 |
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author | Wang, Yong-Xia Zhu, Hui-Fang Zhang, Zhe-Ying Ren, Feng Hu, Yu-Han |
author_facet | Wang, Yong-Xia Zhu, Hui-Fang Zhang, Zhe-Ying Ren, Feng Hu, Yu-Han |
author_sort | Wang, Yong-Xia |
collection | PubMed |
description | BACKGROUND: Growing evidence suggests that MiRNAs play essential roles in the initiation and progression of colorectal cancer (CRC). The aberrant expression of miR-384 has been reported in some cancers. However, the role and mechanism of miR-384 in CRC proliferation remains unknown. METHODS: The expression of miR-384 was detected in CRC and their paired normal tissues by real-time PCR. In vivo and in vitro assays were conducted to confirm the role of miR-384 in the proliferation of CRC. Bioinformatics analysis, luciferase reporter assays, western blot and in vitro assays were used to confirm that AKT3 was the target gene of miR-384. Finally, Spearman’s correlation analyses was carried out to analyze the relationship between miR-384 expression and AKT3 expression in CRC. RESULTS: MiR-384 was down‑regulated in CRC tissues. The in vivo and vitro functional assays verified that the ectopic upregulation of miR-384 inhibited the proliferation of CRC and the inhibition of miR-384 promoted the proliferation of CRC. Bioinformatics analysis, luciferase reporter assays, western blot and in vitro functional assays confirmed AKT3 as the target gene of miR-384. The expression of miR-384 was negatively correlated with the expressions of AKT3. CONCLUSION: Our study verified that miR-384 could significantly suppress the proliferation of CRC by directing targeting AKT3. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s12935-018-0628-6) contains supplementary material, which is available to authorized users. |
format | Online Article Text |
id | pubmed-6122463 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-61224632018-09-05 MiR-384 inhibits the proliferation of colorectal cancer by targeting AKT3 Wang, Yong-Xia Zhu, Hui-Fang Zhang, Zhe-Ying Ren, Feng Hu, Yu-Han Cancer Cell Int Primary Research BACKGROUND: Growing evidence suggests that MiRNAs play essential roles in the initiation and progression of colorectal cancer (CRC). The aberrant expression of miR-384 has been reported in some cancers. However, the role and mechanism of miR-384 in CRC proliferation remains unknown. METHODS: The expression of miR-384 was detected in CRC and their paired normal tissues by real-time PCR. In vivo and in vitro assays were conducted to confirm the role of miR-384 in the proliferation of CRC. Bioinformatics analysis, luciferase reporter assays, western blot and in vitro assays were used to confirm that AKT3 was the target gene of miR-384. Finally, Spearman’s correlation analyses was carried out to analyze the relationship between miR-384 expression and AKT3 expression in CRC. RESULTS: MiR-384 was down‑regulated in CRC tissues. The in vivo and vitro functional assays verified that the ectopic upregulation of miR-384 inhibited the proliferation of CRC and the inhibition of miR-384 promoted the proliferation of CRC. Bioinformatics analysis, luciferase reporter assays, western blot and in vitro functional assays confirmed AKT3 as the target gene of miR-384. The expression of miR-384 was negatively correlated with the expressions of AKT3. CONCLUSION: Our study verified that miR-384 could significantly suppress the proliferation of CRC by directing targeting AKT3. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s12935-018-0628-6) contains supplementary material, which is available to authorized users. BioMed Central 2018-09-03 /pmc/articles/PMC6122463/ /pubmed/30186040 http://dx.doi.org/10.1186/s12935-018-0628-6 Text en © The Author(s) 2018 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 Wang, Yong-Xia Zhu, Hui-Fang Zhang, Zhe-Ying Ren, Feng Hu, Yu-Han MiR-384 inhibits the proliferation of colorectal cancer by targeting AKT3 |
title | MiR-384 inhibits the proliferation of colorectal cancer by targeting AKT3 |
title_full | MiR-384 inhibits the proliferation of colorectal cancer by targeting AKT3 |
title_fullStr | MiR-384 inhibits the proliferation of colorectal cancer by targeting AKT3 |
title_full_unstemmed | MiR-384 inhibits the proliferation of colorectal cancer by targeting AKT3 |
title_short | MiR-384 inhibits the proliferation of colorectal cancer by targeting AKT3 |
title_sort | mir-384 inhibits the proliferation of colorectal cancer by targeting akt3 |
topic | Primary Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6122463/ https://www.ncbi.nlm.nih.gov/pubmed/30186040 http://dx.doi.org/10.1186/s12935-018-0628-6 |
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