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miR-128-3p serves as an oncogenic microRNA in osteosarcoma cells by downregulating ZC3H12D
Osteosarcoma is the second leading cause of cancer-associated mortality worldwide in children and adolescents. ZC3H12D has been shown to negatively regulate Toll-like receptor signaling and serves as a possible tumor suppressor gene. MicroRNAs (miRNAs/miRs) are known to play an important role in the...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7798096/ https://www.ncbi.nlm.nih.gov/pubmed/33552270 http://dx.doi.org/10.3892/ol.2020.12413 |
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author | Zhu, Maoshu Wu, Yulong Wang, Zhaowei Lin, Minghua Su, Bin Li, Chunyang Liang, Fulong Chen, Xinjiang |
author_facet | Zhu, Maoshu Wu, Yulong Wang, Zhaowei Lin, Minghua Su, Bin Li, Chunyang Liang, Fulong Chen, Xinjiang |
author_sort | Zhu, Maoshu |
collection | PubMed |
description | Osteosarcoma is the second leading cause of cancer-associated mortality worldwide in children and adolescents. ZC3H12D has been shown to negatively regulate Toll-like receptor signaling and serves as a possible tumor suppressor gene. MicroRNAs (miRNAs/miRs) are known to play an important role in the proliferation of human osteosarcoma cells. However, whether miRNAs can affect tumor development by regulating the expression of ZC3H12D has not yet been investigated. The aim of the present study was to investigate the role of miR128-3p in regulating ZC3H12D expression, as well as its function in tumor cell proliferation, apoptosis, and metastasis. Reverse transcription-quantitative PCR, western blotting and dual luciferase reporter assays were performed to analyze the regulation of ZC3H12D expression by miR-128-3p. MTT, colony formation and flow cytometry assays were also used to analyze the effect of miR-128-3p on cell proliferation and apoptosis. A wound healing assay was performed to investigate the cell migration ability. The results demonstrated that miR-128-3p directly targeted ZC3H12D and downregulated its expression, thereby promoting cell proliferation and migration. miR-128-3p overexpression also improved resistance to cisplatin in MG-63 and 143B cell lines, supporting the hypothesis that miR-128-3p may function as an oncogene in osteosarcoma cells. The potential clinical significance of miR-128-3p as a biomarker and therapeutic target provides rationale for further investigation into the miR-128-3p-mediated molecular pathway and how it is associated with osteosarcoma development. |
format | Online Article Text |
id | pubmed-7798096 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-77980962021-02-04 miR-128-3p serves as an oncogenic microRNA in osteosarcoma cells by downregulating ZC3H12D Zhu, Maoshu Wu, Yulong Wang, Zhaowei Lin, Minghua Su, Bin Li, Chunyang Liang, Fulong Chen, Xinjiang Oncol Lett Articles Osteosarcoma is the second leading cause of cancer-associated mortality worldwide in children and adolescents. ZC3H12D has been shown to negatively regulate Toll-like receptor signaling and serves as a possible tumor suppressor gene. MicroRNAs (miRNAs/miRs) are known to play an important role in the proliferation of human osteosarcoma cells. However, whether miRNAs can affect tumor development by regulating the expression of ZC3H12D has not yet been investigated. The aim of the present study was to investigate the role of miR128-3p in regulating ZC3H12D expression, as well as its function in tumor cell proliferation, apoptosis, and metastasis. Reverse transcription-quantitative PCR, western blotting and dual luciferase reporter assays were performed to analyze the regulation of ZC3H12D expression by miR-128-3p. MTT, colony formation and flow cytometry assays were also used to analyze the effect of miR-128-3p on cell proliferation and apoptosis. A wound healing assay was performed to investigate the cell migration ability. The results demonstrated that miR-128-3p directly targeted ZC3H12D and downregulated its expression, thereby promoting cell proliferation and migration. miR-128-3p overexpression also improved resistance to cisplatin in MG-63 and 143B cell lines, supporting the hypothesis that miR-128-3p may function as an oncogene in osteosarcoma cells. The potential clinical significance of miR-128-3p as a biomarker and therapeutic target provides rationale for further investigation into the miR-128-3p-mediated molecular pathway and how it is associated with osteosarcoma development. D.A. Spandidos 2021-02 2020-12-31 /pmc/articles/PMC7798096/ /pubmed/33552270 http://dx.doi.org/10.3892/ol.2020.12413 Text en Copyright: © Zhu 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 Zhu, Maoshu Wu, Yulong Wang, Zhaowei Lin, Minghua Su, Bin Li, Chunyang Liang, Fulong Chen, Xinjiang miR-128-3p serves as an oncogenic microRNA in osteosarcoma cells by downregulating ZC3H12D |
title | miR-128-3p serves as an oncogenic microRNA in osteosarcoma cells by downregulating ZC3H12D |
title_full | miR-128-3p serves as an oncogenic microRNA in osteosarcoma cells by downregulating ZC3H12D |
title_fullStr | miR-128-3p serves as an oncogenic microRNA in osteosarcoma cells by downregulating ZC3H12D |
title_full_unstemmed | miR-128-3p serves as an oncogenic microRNA in osteosarcoma cells by downregulating ZC3H12D |
title_short | miR-128-3p serves as an oncogenic microRNA in osteosarcoma cells by downregulating ZC3H12D |
title_sort | mir-128-3p serves as an oncogenic microrna in osteosarcoma cells by downregulating zc3h12d |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7798096/ https://www.ncbi.nlm.nih.gov/pubmed/33552270 http://dx.doi.org/10.3892/ol.2020.12413 |
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