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- Jiafeng Li, Huixin Liu, Qiwang Lin, Huajiao Chen, Liya Liu, Hongjuan Liao, Ying Cheng, Xiuli Zhang, Zhenlong Wang, Aling Shen, and Guolong Chen.
- Department of pharmacy department, Fujian Maternity and Child Health Hospital, Fuzhou, Fujian, China.
- Medicine (Baltimore). 2022 Nov 18; 101 (46): e29328e29328.
AbstractMetastasis is the major cause of death and failure of cancer chemotherapy in patients with breast cancer (BC). Activation of TGF-β/lncRNA-MALAT1/miR-200c has been reported to play an essential role during the metastasis of BC cells. The present study aimed to validate the suppression of BC-cell migration and invasion by baicalin and explore its regulatory effects on the TGF-β/lncRNA-MALAT1/miR-200c signaling pathway. We found that baicalin treatment inhibited cell viability and migration and invasion. Mechanistically, baicalin treatment significantly downregulated the expression of TGF-β, ZEB1, and N-cadherin and upregulated E-cadherin on both mRNA and protein levels. Additionally, baicalin treatment significantly downregulated the expression of lncRNA-MALAT1 and upregulated that of miR-200c. Collectively, baicalin significantly suppresses cell viability, migration, and invasion of BC cells possibly by regulating the TGF-β/lncRNA-MALAT1/miR-200c pathway.Copyright © 2022 the Author(s). Published by Wolters Kluwer Health, Inc.
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