Pien Tze Huang () Overcomes Doxorubicin Resistance and Inhibits Epithelial-Mesenchymal Transition in MCF-7/ADR Cells.
10.1007/s11655-018-2992-4
- Author:
Xi CHEN
1
;
Fei QI
1
;
A-Ling SHEN
1
;
Jian-Feng CHU
1
;
Thomas Joseph SFERRA
2
;
You-Qin CHEN
1
;
Jun PENG
3
Author Information
1. Academy of Integrative Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou, 350122, China.
2. School of Medicine, Case Western Reserve University, Cleveland, OH, 44106, USA.
3. Academy of Integrative Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou, 350122, China. pjunlab@hotmail.com.
- Publication Type:Journal Article
- Keywords:
Chinese medicine;
Pien Tze Huang;
breast cancer;
chemoresistance;
epithelial-mesenchymal transition
- From:
Chinese journal of integrative medicine
2019;25(8):598-603
- CountryChina
- Language:English
-
Abstract:
OBJECTIVE:To evaluate the effect of Pien Tze Huang (, PZH) on breast cancer chemoresistance and related epithelial-mesenchymal transition (EMT) and investigate the underlying mechanisms.
METHODS:3-(4,5-Dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay was used to determine the cell viability. Adriamycin (ADR) staining observed by fluorescence microscope was performed to detect the accumulation of ADR. Transwell assay was used to analyze the cell migration and invasion. Western-blot was performed to detect the protein expression of related genes.
RESULTS:MCF-7/ADR cells were resistant to ADR treatment, and PZH treatment inhibited the viability of MCF-7/ADR cells in a dose-dependent manner. PZH treatment also increased the intercellular accumulation of ADR and down-regulated the expression of ABCG2 and ABCB1 in MCF-7/ADR cells (P<0.05). In addition, PZH treatment inhibited EMT, migration and invasion of MCF-7/ADR cells (P<0.05). Moreover, PZH suppressed activation of transforming growth factor β1 (TGF-β) signaling in MCF-7/ADR cells (P<0.05).
CONCLUSION:PZH treatment can effectively overcome chemoresistance via down regulating ABCG2, ABCB1 and inhibit EMT in ADR resistant human breast cancer cells via suppression of the TGF-β1 pathway.
