Abstract
Epithelial-mesenchymal transition (EMT) is the first step required for breast cancer to initiate metastasis. However, the potential of drugs to block and reverse the EMT process are not well explored. In the present study, we investigated the inhibitory effect of beta-elemene (ELE), an active component of a natural plant-derived anti-neoplastic agent in an established EMT model mediated by transforming growth factor-beta1 (TGF-β1). We found that ELE (40 µg/ml ) blocked the TGF-β1-induced phenotypic transition in the human breast cancer cell line MCF-7. ELE was able to inhibit TGF-β1-mediated upregulation of mRNA and protein expression of nuclear transcription factors (SNAI1, SNAI2, TWIST and SIP1), potentially through decreasing the expression and phosphorylation of Smad3, a central protein mediating the TGF-β1 signalling pathway. These findings suggest a potential therapeutic benefit of ELE in treating basal-like breast cancer.
Highlights
Breast cancer is the most commonly diagnosed cancer, and the second leading cause of cancer-related deaths in US women [1]
Using an epithelial-mesenchymal transition (EMT) model of the breast cancer cell line MCF-7 treated with transforming growth factor-beta1 (TGF-b1), we examined the effect of ELE on EMTrelated phenotypic and gene expression changes
These data confirmed that TGF-b1 treatment results in EMT in MCF-7 cells
Summary
Breast cancer is the most commonly diagnosed cancer, and the second leading cause of cancer-related deaths in US women [1]. Metastasis is often a lethal component of breast cancer, while other patients die from long-term recurrence [2]. Several steps are involved in cancer metastasis, including epithelial-mesenchymal transition (EMT), invasion, intravasation, adhesion, extravasation and mesenchymal-epithelial transition (MET) [3,4]. There has been growing interest in investigating the role of EMT in cancer metastasis, as it is the first step in the migration of breast cancer cells [5,6,7,8]. Recent evidence indicates that EMT is associated with cancer cell stemness, chemoresistance and circulating tumor cells in breast cancer [9,10,11,12]. Inhibition of EMT may provide therapeutic potential for improving the prognosis of breast cancer patients
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