期刊
MEDICINE
卷 101, 期 46, 页码 -出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/MD.0000000000029328
关键词
baicalin; breast cancer; invasion; migration; TGF-beta; lncRNA-MALAT1; miR-200c
This study validates the suppression of breast cancer cell migration and invasion by baicalin through regulating the TGF-beta/lncRNA-MALAT1/miR-200c pathway.
Metastasis is the major cause of death and failure of cancer chemotherapy in patients with breast cancer (BC). Activation of TGF-beta/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-beta/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-beta, 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-beta/lncRNA-MALAT1/miR-200c pathway.
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