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Promotion of ovarian cancer cell invasion, migration and colony formation by the miR-21/Wnt/CD44v6 pathway
Ovarian cancer (OC) has the highest mortality rate among female malignant tumors, and OC commonly relapses and metastasizes. The mechanisms underlying the occurrence and development of ovarian cancer are numerous and complicated. The aim of the present study was to explore an important molecular mec...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6549100/ https://www.ncbi.nlm.nih.gov/pubmed/31115569 http://dx.doi.org/10.3892/or.2019.7153 |
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author | Wang, Yanqing Yang, Xiao Yuan, Mengqin Xian, Shu Zhang, Li Yang, Dongyong Cheng, Yanxiang |
author_facet | Wang, Yanqing Yang, Xiao Yuan, Mengqin Xian, Shu Zhang, Li Yang, Dongyong Cheng, Yanxiang |
author_sort | Wang, Yanqing |
collection | PubMed |
description | Ovarian cancer (OC) has the highest mortality rate among female malignant tumors, and OC commonly relapses and metastasizes. The mechanisms underlying the occurrence and development of ovarian cancer are numerous and complicated. The aim of the present study was to explore an important molecular mechanism that may provide a theoretical basis for the clinical treatment of ovarian cancer. In the present study, the expression level of miR-21 was analyzed in clinical specimens, normal ovarian epithelial cells and three different ovarian cancer epithelial cell lines. Then, in vitro experiments were performed following the transient transfection of miR-21 mimics and inhibitors into SKOV3 cells. RT-PCR, western blot analysis, colony formation assay, and Transwell migration and invasion assays were used to explore the role of miR-21 in ovarian cancer. In addition, Wnt signaling pathway inhibitors and activators were used to validate the hypothesis that the miR-21/Wnt/CD44v6 pathway plays an important role in OC. In ovarian cancer tissues and cells, miR-21 was highly expressed, and the high expression of miR-21 could activate the Wnt signaling pathway to regulate the expression of CD44v6 and affect the proliferation, invasion and migration of OC cells. miR-21 regulated the expression of CD44v6 by activating the Wnt signaling pathway, which plays an important role in the development of ovarian cancer. These findings provide a potential new therapeutic target for the clinical diagnosis and treatment of ovarian cancer. |
format | Online Article Text |
id | pubmed-6549100 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-65491002019-06-10 Promotion of ovarian cancer cell invasion, migration and colony formation by the miR-21/Wnt/CD44v6 pathway Wang, Yanqing Yang, Xiao Yuan, Mengqin Xian, Shu Zhang, Li Yang, Dongyong Cheng, Yanxiang Oncol Rep Articles Ovarian cancer (OC) has the highest mortality rate among female malignant tumors, and OC commonly relapses and metastasizes. The mechanisms underlying the occurrence and development of ovarian cancer are numerous and complicated. The aim of the present study was to explore an important molecular mechanism that may provide a theoretical basis for the clinical treatment of ovarian cancer. In the present study, the expression level of miR-21 was analyzed in clinical specimens, normal ovarian epithelial cells and three different ovarian cancer epithelial cell lines. Then, in vitro experiments were performed following the transient transfection of miR-21 mimics and inhibitors into SKOV3 cells. RT-PCR, western blot analysis, colony formation assay, and Transwell migration and invasion assays were used to explore the role of miR-21 in ovarian cancer. In addition, Wnt signaling pathway inhibitors and activators were used to validate the hypothesis that the miR-21/Wnt/CD44v6 pathway plays an important role in OC. In ovarian cancer tissues and cells, miR-21 was highly expressed, and the high expression of miR-21 could activate the Wnt signaling pathway to regulate the expression of CD44v6 and affect the proliferation, invasion and migration of OC cells. miR-21 regulated the expression of CD44v6 by activating the Wnt signaling pathway, which plays an important role in the development of ovarian cancer. These findings provide a potential new therapeutic target for the clinical diagnosis and treatment of ovarian cancer. D.A. Spandidos 2019-07 2019-05-09 /pmc/articles/PMC6549100/ /pubmed/31115569 http://dx.doi.org/10.3892/or.2019.7153 Text en Copyright: © Wang 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 Wang, Yanqing Yang, Xiao Yuan, Mengqin Xian, Shu Zhang, Li Yang, Dongyong Cheng, Yanxiang Promotion of ovarian cancer cell invasion, migration and colony formation by the miR-21/Wnt/CD44v6 pathway |
title | Promotion of ovarian cancer cell invasion, migration and colony formation by the miR-21/Wnt/CD44v6 pathway |
title_full | Promotion of ovarian cancer cell invasion, migration and colony formation by the miR-21/Wnt/CD44v6 pathway |
title_fullStr | Promotion of ovarian cancer cell invasion, migration and colony formation by the miR-21/Wnt/CD44v6 pathway |
title_full_unstemmed | Promotion of ovarian cancer cell invasion, migration and colony formation by the miR-21/Wnt/CD44v6 pathway |
title_short | Promotion of ovarian cancer cell invasion, migration and colony formation by the miR-21/Wnt/CD44v6 pathway |
title_sort | promotion of ovarian cancer cell invasion, migration and colony formation by the mir-21/wnt/cd44v6 pathway |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6549100/ https://www.ncbi.nlm.nih.gov/pubmed/31115569 http://dx.doi.org/10.3892/or.2019.7153 |
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