Affordable Access

deepdyve-link
Publisher Website

Curcumin suppresses doxorubicin-induced epithelial-mesenchymal transition via the inhibition of TGF-β and PI3K/AKT signaling pathways in triple-negative breast cancer cells.

Authors
  • Chen, Wei-Chih
  • Lai, Ying-An
  • Lin, Ying-Chao
  • Ma, Jui-Wen
  • Huang, Li-Fen
  • Yang, Ning-Sun
  • Ho, Chi-Tang
  • Kuo, Sheng-Chu
  • Way, Tzong-Der
Type
Published Article
Journal
Journal of Agricultural and Food Chemistry
Publisher
American Chemical Society
Publication Date
Dec 04, 2013
Volume
61
Issue
48
Pages
11817–11824
Identifiers
DOI: 10.1021/jf404092f
PMID: 24236784
Source
Medline
License
Unknown

Abstract

Triple-negative breast cancer (TNBC) is defined by a lack of expression of the estrogen receptor (ER), progesterone receptor (PR), and epidermal growth factor receptor 2 (HER 2). Therefore, targeted therapy agents may not be used, and therapy is largely limited to chemotherapy. Doxorubicin treatment consequently acquires undesired malignance characteristics [i.e., epithelial-mesenchymal transition (EMT) and multi-drug resistance]. Our results illustrated that doxorubicin triggered EMT and resulted in the acquisition of a mesenchymal phenotype in TNBC cells. Moreover, we found that transforming growth factor-β (TGF-β) and PI3K/AKT signaling pathways were acquired for doxorubicin-induced EMT. Interestingly, we found that curcumin suppressed doxorubicin-induced EMT. Curcumin reversed doxorubicin-induced morphological changes, inhibited doxorubicin-induced downregulation of E-cadherin expressions, and inhibited doxorubicin-induced upregulation of vimentin expression. We also found that curcumin inhibited doxorubicin-induced EMT by inhibiting the TGF-β and PI3K/AKT signaling pathways. Moreover, curcumin enhanced the antiproliferative effects of doxorubicin in TNBC cells. In summary, our results suggest that doxorubicin in combination with curcumin may be a potential therapy for TNBC.

Report this publication

Statistics

Seen <100 times