Propofol inhibits proliferation and epithelial-mesenchymal transition of MCF-7 cells by suppressing miR-21 expression
Breast cancer is a common malignant tumor with a high incidence of recurrence and metastasis. It has been reported that propofol has certain anti-breast cancer effects, but the intrinsic molecular mechanism remains unclear. This study investigated the effect of propofol on breast cancer MCF-7 cells...
| Main Authors: | , , , , , |
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| Format: | Article |
| Language: | English |
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Taylor & Francis Group
2019-12-01
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| Series: | Artificial Cells, Nanomedicine, and Biotechnology |
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| Online Access: | https://www.tandfonline.com/doi/10.1080/21691401.2019.1594000 |
| _version_ | 1818008776412758016 |
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| author | Qing Du Xuezhi Zhang Xin Zhang Ming Wei Hongmei Xu Shilei Wang |
| author_facet | Qing Du Xuezhi Zhang Xin Zhang Ming Wei Hongmei Xu Shilei Wang |
| author_sort | Qing Du |
| collection | DOAJ |
| description | Breast cancer is a common malignant tumor with a high incidence of recurrence and metastasis. It has been reported that propofol has certain anti-breast cancer effects, but the intrinsic molecular mechanism remains unclear. This study investigated the effect of propofol on breast cancer MCF-7 cells and its possible regulatory mechanisms. MCF-7 cells were treated by propofol, and then the effects of propofol on cell growth and epithelial-mesenchymal transition (EMT) were studied. We subsequently testified whether miR-21 was a downstream effector of propofol. As a result, propofol repressed the proliferation and migration of MCF-7 cells, but significantly induced apoptosis. Meanwhile, miR-21 expression and EMT were inhibited by propofol stimulation. The effects of propofol on MCF-7 cells proliferation, apoptosis and EMT were all attenuated when miR-21 was overexpressed. Besides this, the activation of PI3K/AKT and Wnt3a/β-catenin pathways was reduced by propofol stimulation in a miR-21-depedent manner. In conclusion, propofol can inhibit the proliferation and EMT of MCF-7 cells by down-regulating miR-21 expression. Moreover, miR-21 can further regulate PI3K/AKT and Wnt/β-catenin pathways. |
| first_indexed | 2024-04-14T05:33:40Z |
| format | Article |
| id | doaj.art-359e491954534b0ea3c31f642e4d604c |
| institution | Directory Open Access Journal |
| issn | 2169-1401 2169-141X |
| language | English |
| last_indexed | 2024-04-14T05:33:40Z |
| publishDate | 2019-12-01 |
| publisher | Taylor & Francis Group |
| record_format | Article |
| series | Artificial Cells, Nanomedicine, and Biotechnology |
| spelling | doaj.art-359e491954534b0ea3c31f642e4d604c2022-12-22T02:09:43ZengTaylor & Francis GroupArtificial Cells, Nanomedicine, and Biotechnology2169-14012169-141X2019-12-014711265127110.1080/21691401.2019.1594000Propofol inhibits proliferation and epithelial-mesenchymal transition of MCF-7 cells by suppressing miR-21 expressionQing Du0Xuezhi Zhang1Xin Zhang2Ming Wei3Hongmei Xu4Shilei Wang5Department of Anesthesiology, The Affiliated Hospital of Qingdao University, Qingdao, ChinaEmergency Department, The Affiliated Hospital of Qingdao University, Qingdao, ChinaDepartment of Anesthesiology, The Affiliated Hospital of Qingdao University, Qingdao, ChinaDepartment of Anesthesiology, The Affiliated Hospital of Qingdao University, Qingdao, ChinaDepartment of Anesthesiology, The Affiliated Hospital of Qingdao University, Qingdao, ChinaDepartment of Anesthesiology, The Affiliated Hospital of Qingdao University, Qingdao, ChinaBreast cancer is a common malignant tumor with a high incidence of recurrence and metastasis. It has been reported that propofol has certain anti-breast cancer effects, but the intrinsic molecular mechanism remains unclear. This study investigated the effect of propofol on breast cancer MCF-7 cells and its possible regulatory mechanisms. MCF-7 cells were treated by propofol, and then the effects of propofol on cell growth and epithelial-mesenchymal transition (EMT) were studied. We subsequently testified whether miR-21 was a downstream effector of propofol. As a result, propofol repressed the proliferation and migration of MCF-7 cells, but significantly induced apoptosis. Meanwhile, miR-21 expression and EMT were inhibited by propofol stimulation. The effects of propofol on MCF-7 cells proliferation, apoptosis and EMT were all attenuated when miR-21 was overexpressed. Besides this, the activation of PI3K/AKT and Wnt3a/β-catenin pathways was reduced by propofol stimulation in a miR-21-depedent manner. In conclusion, propofol can inhibit the proliferation and EMT of MCF-7 cells by down-regulating miR-21 expression. Moreover, miR-21 can further regulate PI3K/AKT and Wnt/β-catenin pathways.https://www.tandfonline.com/doi/10.1080/21691401.2019.1594000PropofolMCF-7epithelial-mesenchymal transition (EMT)miR-21 |
| spellingShingle | Qing Du Xuezhi Zhang Xin Zhang Ming Wei Hongmei Xu Shilei Wang Propofol inhibits proliferation and epithelial-mesenchymal transition of MCF-7 cells by suppressing miR-21 expression Artificial Cells, Nanomedicine, and Biotechnology Propofol MCF-7 epithelial-mesenchymal transition (EMT) miR-21 |
| title | Propofol inhibits proliferation and epithelial-mesenchymal transition of MCF-7 cells by suppressing miR-21 expression |
| title_full | Propofol inhibits proliferation and epithelial-mesenchymal transition of MCF-7 cells by suppressing miR-21 expression |
| title_fullStr | Propofol inhibits proliferation and epithelial-mesenchymal transition of MCF-7 cells by suppressing miR-21 expression |
| title_full_unstemmed | Propofol inhibits proliferation and epithelial-mesenchymal transition of MCF-7 cells by suppressing miR-21 expression |
| title_short | Propofol inhibits proliferation and epithelial-mesenchymal transition of MCF-7 cells by suppressing miR-21 expression |
| title_sort | propofol inhibits proliferation and epithelial mesenchymal transition of mcf 7 cells by suppressing mir 21 expression |
| topic | Propofol MCF-7 epithelial-mesenchymal transition (EMT) miR-21 |
| url | https://www.tandfonline.com/doi/10.1080/21691401.2019.1594000 |
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