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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...

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Autores principales: Wang, Yong-Xia, Zhu, Hui-Fang, Zhang, Zhe-Ying, Ren, Feng, Hu, Yu-Han
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2018
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.
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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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