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The Effect of miR-361-3p Targeting TRAF6 on Apoptosis of Multiple Myeloma Cells
microRNA-361-3p (miR-361-3p) is involved in the carcinogenesis of oral cancer and pancreatic catheter adenocarcinoma, and has anti-carcinogenic effects on non-small cell lung cancer (NSCLC). However, its effect on multiple myeloma (MM) is less reported. Here, we found that upregulating the expressio...
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Korean Society for Microbiology and Biotechnology
2021
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9705904/ https://www.ncbi.nlm.nih.gov/pubmed/33323675 http://dx.doi.org/10.4014/jmb.2010.10059 |
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author | Fan, Zhen Wu, Zhiwei Yang, Bo |
author_facet | Fan, Zhen Wu, Zhiwei Yang, Bo |
author_sort | Fan, Zhen |
collection | PubMed |
description | microRNA-361-3p (miR-361-3p) is involved in the carcinogenesis of oral cancer and pancreatic catheter adenocarcinoma, and has anti-carcinogenic effects on non-small cell lung cancer (NSCLC). However, its effect on multiple myeloma (MM) is less reported. Here, we found that upregulating the expression of miR-361-3p inhibited MM cell viability and promoted MM apoptosis. We measured expressions of tumor necrosis factor receptor-associated factor 6 (TRAF6) and miR-361-3p in MM cells and detected the viability, colony formation rate, and apoptosis of MM cells. In addition, we measured expressions of apoptosis-related genes Bcl-2, Bax, and Cleaved caspase-3 (C caspase-3). The binding site between miR-361-3p and TRAF6 was predicted by TargetScan. Our results showed that miR-361-3p was low expressed in the plasma of MM patients and cell lines, while its overexpression inhibited viability and colony formation of MM cells and increased the cell apoptosis. Furthermore, TRAF6, which was predicted to be a target gene of miR-361-3p, was highexpressed in the plasma of patients and cell lines with MM. Rescue experiments demonstrated that the effect of TRAF6 on MM cells was opposite to that of miR-361-3p. Upregulation of miR-361-3p induced apoptosis and inhibited the proliferation of MM cells through targeting TRAF6, suggesting that miR-361-3p might be a potential target for MM therapy. |
format | Online Article Text |
id | pubmed-9705904 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Korean Society for Microbiology and Biotechnology |
record_format | MEDLINE/PubMed |
spelling | pubmed-97059042022-12-13 The Effect of miR-361-3p Targeting TRAF6 on Apoptosis of Multiple Myeloma Cells Fan, Zhen Wu, Zhiwei Yang, Bo J Microbiol Biotechnol Research article microRNA-361-3p (miR-361-3p) is involved in the carcinogenesis of oral cancer and pancreatic catheter adenocarcinoma, and has anti-carcinogenic effects on non-small cell lung cancer (NSCLC). However, its effect on multiple myeloma (MM) is less reported. Here, we found that upregulating the expression of miR-361-3p inhibited MM cell viability and promoted MM apoptosis. We measured expressions of tumor necrosis factor receptor-associated factor 6 (TRAF6) and miR-361-3p in MM cells and detected the viability, colony formation rate, and apoptosis of MM cells. In addition, we measured expressions of apoptosis-related genes Bcl-2, Bax, and Cleaved caspase-3 (C caspase-3). The binding site between miR-361-3p and TRAF6 was predicted by TargetScan. Our results showed that miR-361-3p was low expressed in the plasma of MM patients and cell lines, while its overexpression inhibited viability and colony formation of MM cells and increased the cell apoptosis. Furthermore, TRAF6, which was predicted to be a target gene of miR-361-3p, was highexpressed in the plasma of patients and cell lines with MM. Rescue experiments demonstrated that the effect of TRAF6 on MM cells was opposite to that of miR-361-3p. Upregulation of miR-361-3p induced apoptosis and inhibited the proliferation of MM cells through targeting TRAF6, suggesting that miR-361-3p might be a potential target for MM therapy. Korean Society for Microbiology and Biotechnology 2021-02-28 2020-12-14 /pmc/articles/PMC9705904/ /pubmed/33323675 http://dx.doi.org/10.4014/jmb.2010.10059 Text en Copyright © 2021 by The Korean Society for Microbiology and Biotechnology https://creativecommons.org/licenses/by/4.0/This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Research article Fan, Zhen Wu, Zhiwei Yang, Bo The Effect of miR-361-3p Targeting TRAF6 on Apoptosis of Multiple Myeloma Cells |
title | The Effect of miR-361-3p Targeting TRAF6 on Apoptosis of Multiple Myeloma Cells |
title_full | The Effect of miR-361-3p Targeting TRAF6 on Apoptosis of Multiple Myeloma Cells |
title_fullStr | The Effect of miR-361-3p Targeting TRAF6 on Apoptosis of Multiple Myeloma Cells |
title_full_unstemmed | The Effect of miR-361-3p Targeting TRAF6 on Apoptosis of Multiple Myeloma Cells |
title_short | The Effect of miR-361-3p Targeting TRAF6 on Apoptosis of Multiple Myeloma Cells |
title_sort | effect of mir-361-3p targeting traf6 on apoptosis of multiple myeloma cells |
topic | Research article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9705904/ https://www.ncbi.nlm.nih.gov/pubmed/33323675 http://dx.doi.org/10.4014/jmb.2010.10059 |
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