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MicroRNA-196a promotes cell proliferation and inhibits apoptosis in human ovarian cancer by directly targeting DDX3 and regulating the PTEN/PI3K/AKT signaling pathway
MicroRNAs (miRNAs/miRs) are small noncoding RNAs 19–24 nucleotides in length, which can play an important role in tumor development. However, the influence of miRNAs on the tumorigenicity of ovarian cancer cells has not been fully elucidated. Previously, DEAD box protein (DDX) 1 has been shown to pl...
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/PMC7339644/ https://www.ncbi.nlm.nih.gov/pubmed/32626994 http://dx.doi.org/10.3892/mmr.2020.11236 |
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author | Ni, Jie Chen, Li Ling, Li Wu, Mengfei Ren, Qiongzhen Zhu, Weipei |
author_facet | Ni, Jie Chen, Li Ling, Li Wu, Mengfei Ren, Qiongzhen Zhu, Weipei |
author_sort | Ni, Jie |
collection | PubMed |
description | MicroRNAs (miRNAs/miRs) are small noncoding RNAs 19–24 nucleotides in length, which can play an important role in tumor development. However, the influence of miRNAs on the tumorigenicity of ovarian cancer cells has not been fully elucidated. Previously, DEAD box protein (DDX) 1 has been shown to play a role in tumor suppression of ovarian cancer progression. However, the functions of other DDX members in ovarian cancer development remain largely unknown. In the present study, it was demonstrated that overexpression of miR-196a promoted ovarian cancer cell proliferation. In addition, DDX3 was significantly downregulated in ovarian cancer cell lines relative to the normal ovarian cell line. Moreover, DDX3 was identified as a direct target of miR-196a in ovarian cancer cells. In addition, a preliminary mechanistic investigation indicated that downregulation of DDX3 promoted ovarian cancer cell proliferation through the PTEN/PI3K/AKT pathway. Taken together, this confirmed an association between DDX3 and miR-196a in ovarian cancer, and showed that miR-196a promoted the proliferation of ovarian cancer cells and attenuated apoptosis by downregulating the expression of DDX3 through the PTEN/PI3K/AKT pathway. Overall, the results of the present study suggested that DDX3 could be a novel target for ovarian cancer treatment. |
format | Online Article Text |
id | pubmed-7339644 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-73396442020-07-09 MicroRNA-196a promotes cell proliferation and inhibits apoptosis in human ovarian cancer by directly targeting DDX3 and regulating the PTEN/PI3K/AKT signaling pathway Ni, Jie Chen, Li Ling, Li Wu, Mengfei Ren, Qiongzhen Zhu, Weipei Mol Med Rep Articles MicroRNAs (miRNAs/miRs) are small noncoding RNAs 19–24 nucleotides in length, which can play an important role in tumor development. However, the influence of miRNAs on the tumorigenicity of ovarian cancer cells has not been fully elucidated. Previously, DEAD box protein (DDX) 1 has been shown to play a role in tumor suppression of ovarian cancer progression. However, the functions of other DDX members in ovarian cancer development remain largely unknown. In the present study, it was demonstrated that overexpression of miR-196a promoted ovarian cancer cell proliferation. In addition, DDX3 was significantly downregulated in ovarian cancer cell lines relative to the normal ovarian cell line. Moreover, DDX3 was identified as a direct target of miR-196a in ovarian cancer cells. In addition, a preliminary mechanistic investigation indicated that downregulation of DDX3 promoted ovarian cancer cell proliferation through the PTEN/PI3K/AKT pathway. Taken together, this confirmed an association between DDX3 and miR-196a in ovarian cancer, and showed that miR-196a promoted the proliferation of ovarian cancer cells and attenuated apoptosis by downregulating the expression of DDX3 through the PTEN/PI3K/AKT pathway. Overall, the results of the present study suggested that DDX3 could be a novel target for ovarian cancer treatment. D.A. Spandidos 2020-08 2020-06-15 /pmc/articles/PMC7339644/ /pubmed/32626994 http://dx.doi.org/10.3892/mmr.2020.11236 Text en Copyright: © Ni 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 Ni, Jie Chen, Li Ling, Li Wu, Mengfei Ren, Qiongzhen Zhu, Weipei MicroRNA-196a promotes cell proliferation and inhibits apoptosis in human ovarian cancer by directly targeting DDX3 and regulating the PTEN/PI3K/AKT signaling pathway |
title | MicroRNA-196a promotes cell proliferation and inhibits apoptosis in human ovarian cancer by directly targeting DDX3 and regulating the PTEN/PI3K/AKT signaling pathway |
title_full | MicroRNA-196a promotes cell proliferation and inhibits apoptosis in human ovarian cancer by directly targeting DDX3 and regulating the PTEN/PI3K/AKT signaling pathway |
title_fullStr | MicroRNA-196a promotes cell proliferation and inhibits apoptosis in human ovarian cancer by directly targeting DDX3 and regulating the PTEN/PI3K/AKT signaling pathway |
title_full_unstemmed | MicroRNA-196a promotes cell proliferation and inhibits apoptosis in human ovarian cancer by directly targeting DDX3 and regulating the PTEN/PI3K/AKT signaling pathway |
title_short | MicroRNA-196a promotes cell proliferation and inhibits apoptosis in human ovarian cancer by directly targeting DDX3 and regulating the PTEN/PI3K/AKT signaling pathway |
title_sort | microrna-196a promotes cell proliferation and inhibits apoptosis in human ovarian cancer by directly targeting ddx3 and regulating the pten/pi3k/akt signaling pathway |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7339644/ https://www.ncbi.nlm.nih.gov/pubmed/32626994 http://dx.doi.org/10.3892/mmr.2020.11236 |
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