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Chem Biol Interact. 2016 Mar 25;248:74-81. doi: 10.1016/j.cbi.2016.02.004. Epub 2016 Feb 16.

Salinomycin suppresses TGF-β1-induced epithelial-to-mesenchymal transition in MCF-7 human breast cancer cells.

Author information

1
Department of Pathology, Dalian Medical University, Dalian 116044, PR China.
2
The Key Laboratory of Tumor Stem Cell Research of Liaoning Province, Dalian Medical University, Dalian 116044, PR China.
3
Department of Pathology, Dalian Medical University, Dalian 116044, PR China; The Key Laboratory of Tumor Stem Cell Research of Liaoning Province, Dalian Medical University, Dalian 116044, PR China. Electronic address: lilianhong9177@163.com.

Abstract

Epithelial-to-mesenchymal transition (EMT) is the major cause of breast cancer to initiate invasion and metastasis. Salinomycin (Sal) has been found as an effective chemical compound to kill breast cancer stem cells. However, the effect of Sal on invasion and metastasis of breast cancer is unclear. In the present study, we showed that Sal reversed transforming growth factor-β1 (TGF-β1) induced invasion and metastasis accompanied with down-regulation of MMP-2 by experiments on human breast cancer cell line MCF-7. Sal was able to inhibit TGF-β1-induced EMT phenotypic transition and the activation of key signaling molecules involved in Smad (p-Smad2/3,Snail1) and non-Smad (β-catenin, p-p38 MAPK) signals which cooperatively regulate the induction of EMT. Importantly, in a series of breast cancer specimens, we found strong correlation among E-cadherin expression, β-catenin expression, and the lymph node metastatic potential of breast cancer. Our research suggests that Sal is promised to be a chemotherapeutic drug by suppressing the metastasis of breast cancer.

KEYWORDS:

Breast cancer MCF-7 cells; Epithelial-to-mesenchymal transition; Salinomycin; TGF-β/Non-Smad signaling; TGF-β/Smad signaling

PMID:
26896736
DOI:
10.1016/j.cbi.2016.02.004
[Indexed for MEDLINE]

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