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miR-30a-3p inhibits the proliferation of liver cancer cells by targeting DNMT3a through the PI3K/AKT signaling pathway
MicroRNAs (miRNAs or miRs) are crucial for normal development and maintenance of homeostasis. Dysregulated miRNA expression contributes to numerous pathological conditions, including cancer tumorigenesis. However, a limited number of studies have examined the regulatory effects of miR-30a-3p in tumo...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6924113/ https://www.ncbi.nlm.nih.gov/pubmed/31897176 http://dx.doi.org/10.3892/ol.2019.11179 |
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author | Chen, Qiong Gao, Yuan Yu, Qin Tang, Feng Zhao, Pei-Wei Luo, Su-Kun Lin, Ju-Sheng Mei, Hong |
author_facet | Chen, Qiong Gao, Yuan Yu, Qin Tang, Feng Zhao, Pei-Wei Luo, Su-Kun Lin, Ju-Sheng Mei, Hong |
author_sort | Chen, Qiong |
collection | PubMed |
description | MicroRNAs (miRNAs or miRs) are crucial for normal development and maintenance of homeostasis. Dysregulated miRNA expression contributes to numerous pathological conditions, including cancer tumorigenesis. However, a limited number of studies have examined the regulatory effects of miR-30a-3p in tumorigenesis. Therefore, the present study investigated the mechanistic process of tumorigenesis in liver cancer. The results revealed a high expression of DNA methyltransferase 3a (DNMT3a) and a low expression of miR-30a-3p in HepG2 cells compared with that in the L02 cell line. A luciferase reporter assay demonstrated that DNMT3a is a direct target of miR-30a-3p. In addition, DNMT3a overexpression significantly enhanced cell proliferation, which was reversed by a miR-30a-3p mimic. Similarly, the miR-30a-3p mimic blocked DNMT3a-triggered cell cycle processes and apoptosis by attenuating active p-AKT and p-PI3K in HepG2 cells. In summary, the results of the present study demonstrate that miR-30a-3p is essential for cell proliferation regulation via its association with AKT/PI3K signaling in liver cancer. These results provide insight into the molecular mechanism by which miR-30a-3p inhibits liver cancer cell proliferation and provides a foundation for its clinical development and application. |
format | Online Article Text |
id | pubmed-6924113 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-69241132020-01-02 miR-30a-3p inhibits the proliferation of liver cancer cells by targeting DNMT3a through the PI3K/AKT signaling pathway Chen, Qiong Gao, Yuan Yu, Qin Tang, Feng Zhao, Pei-Wei Luo, Su-Kun Lin, Ju-Sheng Mei, Hong Oncol Lett Articles MicroRNAs (miRNAs or miRs) are crucial for normal development and maintenance of homeostasis. Dysregulated miRNA expression contributes to numerous pathological conditions, including cancer tumorigenesis. However, a limited number of studies have examined the regulatory effects of miR-30a-3p in tumorigenesis. Therefore, the present study investigated the mechanistic process of tumorigenesis in liver cancer. The results revealed a high expression of DNA methyltransferase 3a (DNMT3a) and a low expression of miR-30a-3p in HepG2 cells compared with that in the L02 cell line. A luciferase reporter assay demonstrated that DNMT3a is a direct target of miR-30a-3p. In addition, DNMT3a overexpression significantly enhanced cell proliferation, which was reversed by a miR-30a-3p mimic. Similarly, the miR-30a-3p mimic blocked DNMT3a-triggered cell cycle processes and apoptosis by attenuating active p-AKT and p-PI3K in HepG2 cells. In summary, the results of the present study demonstrate that miR-30a-3p is essential for cell proliferation regulation via its association with AKT/PI3K signaling in liver cancer. These results provide insight into the molecular mechanism by which miR-30a-3p inhibits liver cancer cell proliferation and provides a foundation for its clinical development and application. D.A. Spandidos 2020-01 2019-12-03 /pmc/articles/PMC6924113/ /pubmed/31897176 http://dx.doi.org/10.3892/ol.2019.11179 Text en Copyright: © Chen 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 Chen, Qiong Gao, Yuan Yu, Qin Tang, Feng Zhao, Pei-Wei Luo, Su-Kun Lin, Ju-Sheng Mei, Hong miR-30a-3p inhibits the proliferation of liver cancer cells by targeting DNMT3a through the PI3K/AKT signaling pathway |
title | miR-30a-3p inhibits the proliferation of liver cancer cells by targeting DNMT3a through the PI3K/AKT signaling pathway |
title_full | miR-30a-3p inhibits the proliferation of liver cancer cells by targeting DNMT3a through the PI3K/AKT signaling pathway |
title_fullStr | miR-30a-3p inhibits the proliferation of liver cancer cells by targeting DNMT3a through the PI3K/AKT signaling pathway |
title_full_unstemmed | miR-30a-3p inhibits the proliferation of liver cancer cells by targeting DNMT3a through the PI3K/AKT signaling pathway |
title_short | miR-30a-3p inhibits the proliferation of liver cancer cells by targeting DNMT3a through the PI3K/AKT signaling pathway |
title_sort | mir-30a-3p inhibits the proliferation of liver cancer cells by targeting dnmt3a through the pi3k/akt signaling pathway |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6924113/ https://www.ncbi.nlm.nih.gov/pubmed/31897176 http://dx.doi.org/10.3892/ol.2019.11179 |
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