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Ligustrazine inhibits the proliferation and migration of ovarian cancer cells via regulating miR-211
Ovarian cancer (OC) is a commonly diagnosed female cancer. Ligustrazine (LSZ), a natural compound, has been reported to exert anti-cancer activity, although the mechanisms underlying the anti-cancer effects are not clear. The present study investigated the impact of LSZ on cell proliferation and mig...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Portland Press Ltd.
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7786329/ https://www.ncbi.nlm.nih.gov/pubmed/33245099 http://dx.doi.org/10.1042/BSR20200199 |
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author | Zhang, Hairong Ding, Shichao Xia, Lei |
author_facet | Zhang, Hairong Ding, Shichao Xia, Lei |
author_sort | Zhang, Hairong |
collection | PubMed |
description | Ovarian cancer (OC) is a commonly diagnosed female cancer. Ligustrazine (LSZ), a natural compound, has been reported to exert anti-cancer activity, although the mechanisms underlying the anti-cancer effects are not clear. The present study investigated the impact of LSZ on cell proliferation and migration by regulating microRNA-211 (miR-211) expression using the human ovarian cancer SK-OV-3 and OVCAR-3 cell lines. OC cells were treated with 0, 0.5, 1, and 2 mM LSZ, and quantitative real-time PCR was utilized to measure miR-211 levels in SK-OV-3 and OVCAR-3 cells with different treatment. Moreover, to further confirm the roles of miR-211 in LSZ induced anti-tumor effects, miR-211 expression was inhibited by transfection of miR-211 inhibitors in SK-OV-3 cells. Cell proliferation of transfected cells was evaluated using the CCK-8 and colony formation assay. The scratch assay was employed to assess cell migration and transwell assay was performed for evaluating the cell invasion. Protein levels of epithelial–mesenchymal transition (EMT) markers were determined by Western blotting. We found that LSZ inhibited the viability, proliferation, migration and invasion ability of SK-OV-3 and OVCAR-3 cells in a dose-dependent manner; moreover, LSZ could significantly increase the expression of miR-211 in both SK-OV-3 and OVCAR-3, and knockdown of miR-211 in SK-OV-3 cells partially abrogated the anti-tumor behavior of LSZ by promoting the viability, proliferation, migration, invasion and EMT of SK-OV-3 cells. Thus, we found that LSZ can inhibit the proliferation and migration of OC cells via regulating miR-211. Our study suggests that LSZ might be a potential and effective treatment for OC. |
format | Online Article Text |
id | pubmed-7786329 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Portland Press Ltd. |
record_format | MEDLINE/PubMed |
spelling | pubmed-77863292021-01-13 Ligustrazine inhibits the proliferation and migration of ovarian cancer cells via regulating miR-211 Zhang, Hairong Ding, Shichao Xia, Lei Biosci Rep Cancer Ovarian cancer (OC) is a commonly diagnosed female cancer. Ligustrazine (LSZ), a natural compound, has been reported to exert anti-cancer activity, although the mechanisms underlying the anti-cancer effects are not clear. The present study investigated the impact of LSZ on cell proliferation and migration by regulating microRNA-211 (miR-211) expression using the human ovarian cancer SK-OV-3 and OVCAR-3 cell lines. OC cells were treated with 0, 0.5, 1, and 2 mM LSZ, and quantitative real-time PCR was utilized to measure miR-211 levels in SK-OV-3 and OVCAR-3 cells with different treatment. Moreover, to further confirm the roles of miR-211 in LSZ induced anti-tumor effects, miR-211 expression was inhibited by transfection of miR-211 inhibitors in SK-OV-3 cells. Cell proliferation of transfected cells was evaluated using the CCK-8 and colony formation assay. The scratch assay was employed to assess cell migration and transwell assay was performed for evaluating the cell invasion. Protein levels of epithelial–mesenchymal transition (EMT) markers were determined by Western blotting. We found that LSZ inhibited the viability, proliferation, migration and invasion ability of SK-OV-3 and OVCAR-3 cells in a dose-dependent manner; moreover, LSZ could significantly increase the expression of miR-211 in both SK-OV-3 and OVCAR-3, and knockdown of miR-211 in SK-OV-3 cells partially abrogated the anti-tumor behavior of LSZ by promoting the viability, proliferation, migration, invasion and EMT of SK-OV-3 cells. Thus, we found that LSZ can inhibit the proliferation and migration of OC cells via regulating miR-211. Our study suggests that LSZ might be a potential and effective treatment for OC. Portland Press Ltd. 2021-01-05 /pmc/articles/PMC7786329/ /pubmed/33245099 http://dx.doi.org/10.1042/BSR20200199 Text en © 2021 The Author(s). https://creativecommons.org/licenses/by/4.0/ This is an open access article published by Portland Press Limited on behalf of the Biochemical Society and distributed under the Creative Commons Attribution License 4.0 (CC BY) (https://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Cancer Zhang, Hairong Ding, Shichao Xia, Lei Ligustrazine inhibits the proliferation and migration of ovarian cancer cells via regulating miR-211 |
title | Ligustrazine inhibits the proliferation and migration of ovarian cancer cells via regulating miR-211 |
title_full | Ligustrazine inhibits the proliferation and migration of ovarian cancer cells via regulating miR-211 |
title_fullStr | Ligustrazine inhibits the proliferation and migration of ovarian cancer cells via regulating miR-211 |
title_full_unstemmed | Ligustrazine inhibits the proliferation and migration of ovarian cancer cells via regulating miR-211 |
title_short | Ligustrazine inhibits the proliferation and migration of ovarian cancer cells via regulating miR-211 |
title_sort | ligustrazine inhibits the proliferation and migration of ovarian cancer cells via regulating mir-211 |
topic | Cancer |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7786329/ https://www.ncbi.nlm.nih.gov/pubmed/33245099 http://dx.doi.org/10.1042/BSR20200199 |
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