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MicroRNA-106b functions as an oncogene and regulates tumor viability and metastasis by targeting LARP4B in prostate cancer

Prostate cancer (PCa) is the most common malignancy among males worldwide, and is one of the leading causes of cancer-related mortality. MicroRNAs (miRs) are a type of endogenous, noncoding RNA that serve a key role in pathological processes, and have been demonstrated to be involved in the formatio...

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Autores principales: Yin, Weiqi, Chen, Junfeng, Wang, Guoyao, Zhang, Dongxu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6625195/
https://www.ncbi.nlm.nih.gov/pubmed/31173237
http://dx.doi.org/10.3892/mmr.2019.10343
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author Yin, Weiqi
Chen, Junfeng
Wang, Guoyao
Zhang, Dongxu
author_facet Yin, Weiqi
Chen, Junfeng
Wang, Guoyao
Zhang, Dongxu
author_sort Yin, Weiqi
collection PubMed
description Prostate cancer (PCa) is the most common malignancy among males worldwide, and is one of the leading causes of cancer-related mortality. MicroRNAs (miRs) are a type of endogenous, noncoding RNA that serve a key role in pathological processes, and have been demonstrated to be involved in the formation and progression of PCa. Previous studies have reported that miR-106b acts as an oncogene; however, the specific effects of miR-106b on PCa have not been fully elucidated. The present study aimed to investigate the role and underlying molecular mechanisms of miR-106b in the initiation and progression of PCa. In this study, miR-106b was reported to be overexpressed and la-related protein 4B (LARP4B) was downregulated in PCa tissues compared with paracancerous tissues. In addition, LARP4B was identified as a target gene of miR-106b by bioinformatics prediction analysis and a dual luciferase reporter gene assay. Furthermore, MTT, wound healing and Transwell assays were performed to evaluate PCa cell viability, and migration and invasive abilities. The data revealed that inhibition of miR-106b significantly suppressed the viability, migration and invasion of PCa cells. In addition, inhibition of miR-106b significantly suppressed the mRNA and protein expression of cancer-related genes, including matrix metalloproteinase-2, cluster of differentiation 44 and Ki-67, and increased that of the tumor suppressor, mothers against decapentaplegic homolog 2. Collectively, the findings of the present study indicated that miR-106b may target LAR4B to inhibit cancer cell viability, migration and invasion, and may be considered as a novel therapeutic target in PCa.
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spelling pubmed-66251952019-07-31 MicroRNA-106b functions as an oncogene and regulates tumor viability and metastasis by targeting LARP4B in prostate cancer Yin, Weiqi Chen, Junfeng Wang, Guoyao Zhang, Dongxu Mol Med Rep Articles Prostate cancer (PCa) is the most common malignancy among males worldwide, and is one of the leading causes of cancer-related mortality. MicroRNAs (miRs) are a type of endogenous, noncoding RNA that serve a key role in pathological processes, and have been demonstrated to be involved in the formation and progression of PCa. Previous studies have reported that miR-106b acts as an oncogene; however, the specific effects of miR-106b on PCa have not been fully elucidated. The present study aimed to investigate the role and underlying molecular mechanisms of miR-106b in the initiation and progression of PCa. In this study, miR-106b was reported to be overexpressed and la-related protein 4B (LARP4B) was downregulated in PCa tissues compared with paracancerous tissues. In addition, LARP4B was identified as a target gene of miR-106b by bioinformatics prediction analysis and a dual luciferase reporter gene assay. Furthermore, MTT, wound healing and Transwell assays were performed to evaluate PCa cell viability, and migration and invasive abilities. The data revealed that inhibition of miR-106b significantly suppressed the viability, migration and invasion of PCa cells. In addition, inhibition of miR-106b significantly suppressed the mRNA and protein expression of cancer-related genes, including matrix metalloproteinase-2, cluster of differentiation 44 and Ki-67, and increased that of the tumor suppressor, mothers against decapentaplegic homolog 2. Collectively, the findings of the present study indicated that miR-106b may target LAR4B to inhibit cancer cell viability, migration and invasion, and may be considered as a novel therapeutic target in PCa. D.A. Spandidos 2019-08 2019-06-05 /pmc/articles/PMC6625195/ /pubmed/31173237 http://dx.doi.org/10.3892/mmr.2019.10343 Text en Copyright: © Yin 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
Yin, Weiqi
Chen, Junfeng
Wang, Guoyao
Zhang, Dongxu
MicroRNA-106b functions as an oncogene and regulates tumor viability and metastasis by targeting LARP4B in prostate cancer
title MicroRNA-106b functions as an oncogene and regulates tumor viability and metastasis by targeting LARP4B in prostate cancer
title_full MicroRNA-106b functions as an oncogene and regulates tumor viability and metastasis by targeting LARP4B in prostate cancer
title_fullStr MicroRNA-106b functions as an oncogene and regulates tumor viability and metastasis by targeting LARP4B in prostate cancer
title_full_unstemmed MicroRNA-106b functions as an oncogene and regulates tumor viability and metastasis by targeting LARP4B in prostate cancer
title_short MicroRNA-106b functions as an oncogene and regulates tumor viability and metastasis by targeting LARP4B in prostate cancer
title_sort microrna-106b functions as an oncogene and regulates tumor viability and metastasis by targeting larp4b in prostate cancer
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6625195/
https://www.ncbi.nlm.nih.gov/pubmed/31173237
http://dx.doi.org/10.3892/mmr.2019.10343
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