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MicroRNA-106a suppresses prostate cancer proliferation, migration and invasion by targeting tumor-derived IL-8
BACKGROUND: Tumor-derived interleukin-8 (IL-8) promotes tumorigenesis and progression of prostate cancer (PCa). MicroRNAs (miRNAs) are noncoding regulatory RNAs and their dysregulation is known to be implicated in carcinogenesis. However, the post-transcriptional mechanism of IL-8 via miRNAs is not...
Autores principales: | , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
AME Publishing Company
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8799044/ https://www.ncbi.nlm.nih.gov/pubmed/35117716 http://dx.doi.org/10.21037/tcr.2020.03.70 |
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author | Shen, Pengfei Sun, Guangxi Zhao, Peng Dai, Jindong Zhang, Xingming Zhao, Jinge Zhu, Sha Chen, Junru Tao, Ronggui Yang, Jiyu Zeng, Hao |
author_facet | Shen, Pengfei Sun, Guangxi Zhao, Peng Dai, Jindong Zhang, Xingming Zhao, Jinge Zhu, Sha Chen, Junru Tao, Ronggui Yang, Jiyu Zeng, Hao |
author_sort | Shen, Pengfei |
collection | PubMed |
description | BACKGROUND: Tumor-derived interleukin-8 (IL-8) promotes tumorigenesis and progression of prostate cancer (PCa). MicroRNAs (miRNAs) are noncoding regulatory RNAs and their dysregulation is known to be implicated in carcinogenesis. However, the post-transcriptional mechanism of IL-8 via miRNAs is not fully understood. This study was intended to investigate whether miR-106a could affect the progression of PCa via targeting IL-8 or not. METHODS: Using bioinformatics analysis, we postulated that IL-8 might be post-transcriptionally regulated by miR-106a. This was validated by dual reporter gene assays that miR-106a could bind to the predicted site of IL-8 mRNA. To determine the biological effects of miR-106a on PCa cells (PC-3 and DU145), MTT, terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL), migration and invasion assays were performed. RESULTS: We found that miR-106a was barely expressed in PCa cells, whereas IL-8 was aberrantly upregulated. Elevated miR-106a could reduce IL-8 expression by directly binding the 3'-UTR of IL-8. Overexpression of miR-106a in PCa cells triggered cell apoptosis and suppressed cell proliferation, migration, and invasion. CONCLUSIONS: This research showed that miR-106a could function as a tumor-suppressor by decreasing IL-8 levels in PCa. |
format | Online Article Text |
id | pubmed-8799044 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | AME Publishing Company |
record_format | MEDLINE/PubMed |
spelling | pubmed-87990442022-02-02 MicroRNA-106a suppresses prostate cancer proliferation, migration and invasion by targeting tumor-derived IL-8 Shen, Pengfei Sun, Guangxi Zhao, Peng Dai, Jindong Zhang, Xingming Zhao, Jinge Zhu, Sha Chen, Junru Tao, Ronggui Yang, Jiyu Zeng, Hao Transl Cancer Res Original Article BACKGROUND: Tumor-derived interleukin-8 (IL-8) promotes tumorigenesis and progression of prostate cancer (PCa). MicroRNAs (miRNAs) are noncoding regulatory RNAs and their dysregulation is known to be implicated in carcinogenesis. However, the post-transcriptional mechanism of IL-8 via miRNAs is not fully understood. This study was intended to investigate whether miR-106a could affect the progression of PCa via targeting IL-8 or not. METHODS: Using bioinformatics analysis, we postulated that IL-8 might be post-transcriptionally regulated by miR-106a. This was validated by dual reporter gene assays that miR-106a could bind to the predicted site of IL-8 mRNA. To determine the biological effects of miR-106a on PCa cells (PC-3 and DU145), MTT, terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL), migration and invasion assays were performed. RESULTS: We found that miR-106a was barely expressed in PCa cells, whereas IL-8 was aberrantly upregulated. Elevated miR-106a could reduce IL-8 expression by directly binding the 3'-UTR of IL-8. Overexpression of miR-106a in PCa cells triggered cell apoptosis and suppressed cell proliferation, migration, and invasion. CONCLUSIONS: This research showed that miR-106a could function as a tumor-suppressor by decreasing IL-8 levels in PCa. AME Publishing Company 2020-05 /pmc/articles/PMC8799044/ /pubmed/35117716 http://dx.doi.org/10.21037/tcr.2020.03.70 Text en 2020 Translational Cancer Research. All rights reserved. https://creativecommons.org/licenses/by-nc-nd/4.0/Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/. |
spellingShingle | Original Article Shen, Pengfei Sun, Guangxi Zhao, Peng Dai, Jindong Zhang, Xingming Zhao, Jinge Zhu, Sha Chen, Junru Tao, Ronggui Yang, Jiyu Zeng, Hao MicroRNA-106a suppresses prostate cancer proliferation, migration and invasion by targeting tumor-derived IL-8 |
title | MicroRNA-106a suppresses prostate cancer proliferation, migration and invasion by targeting tumor-derived IL-8 |
title_full | MicroRNA-106a suppresses prostate cancer proliferation, migration and invasion by targeting tumor-derived IL-8 |
title_fullStr | MicroRNA-106a suppresses prostate cancer proliferation, migration and invasion by targeting tumor-derived IL-8 |
title_full_unstemmed | MicroRNA-106a suppresses prostate cancer proliferation, migration and invasion by targeting tumor-derived IL-8 |
title_short | MicroRNA-106a suppresses prostate cancer proliferation, migration and invasion by targeting tumor-derived IL-8 |
title_sort | microrna-106a suppresses prostate cancer proliferation, migration and invasion by targeting tumor-derived il-8 |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8799044/ https://www.ncbi.nlm.nih.gov/pubmed/35117716 http://dx.doi.org/10.21037/tcr.2020.03.70 |
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