Cancer Science | |
Retracted: Glabridin attenuates the migratory and invasive capacity of breast cancer cells by activating microRNA‐200c | |
Xianqing Ye1  Fei Jiang1  Yuan Li1  Juan Mu1  Lu Si1  Xingxing Wang1  Shilong Ning1  | |
[1] Key Laboratory of Modern Toxicology, Ministry of Education, Department of Nutrition and Food Hygiene, School of Public Health, Nanjing Medical University, Nanjing, China | |
关键词: Breast cancer; epithelial‐mesenchymal transition; glabridin; metastasis; microRNA‐200c; | |
DOI : 10.1111/cas.12426 | |
来源: Wiley | |
【 摘 要 】
Current treatments for breast cancer, a common malignancy in human females, are less than satisfactory because of high rates of metastasis. Glabridin (GLA), which acts through the FAK/ROS signaling pathway, has been used as an antioxidant and anti-metastatic agent. However, little is known regarding the effect of microRNA (miRNA) on GLA's anti-metastatic activity. The miRNA-200 family, which is frequently expressed at low levels in triple negative breast cancers, inhibits metastasis by blocking the epithelial–mesenchymal transition. Here, we found that GLA attenuated the migratory and invasive capacity of breast cancer cells by activating miR-200c. GLA induced the mesenchymal–epithelial transition in vitro and in vivo, as determined by increased expression of the epithelial marker, E-cadherin, and decreased expression of the mesenchymal marker, vimentin. Overexpression of miR-200c enhanced the expression of E-cadherin and decreased the expression of vimentin. Furthermore, in MDA-MB-231 and BT-549 breast cancer cells exposed to GLA, knockdown of miR-200c blocked the GLA-induced mesenchymal–epithelial transition and alleviated the GLA-induced inhibition of migration and invasion. Thus, elevation of miR-200c by GLA has considerable therapeutic potential for anti-metastatic therapy for breast cancer patients.Abstract
【 授权许可】
CC BY-NC-ND
© 2014 The Authors. Cancer Science published by Wiley Publishing Asia Pty Ltd on behalf of Japanese Cancer Association.
Creative Commons Attribution-NonCommercial-NoDerivs License, 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.
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