L-arabinose suppresses the epithelial–mesenchymal transition through the autophagy-dependent Wnt/β-catenin signaling pathway in breast cancer

Breast cancer (BC) is one of the major causes of cancer death among women around the world, and the available therapeutic strategies still need to be improved. Monosaccharides, as a natural product, possess the capability to impair the growth of cancer cells, which has been confirmed, but the efficacy of L-arabinose on the epithelial–mesenchymal transition (EMT) of tumor cells remains unclear. In the present study, we found that L-arabinose treatment significantly influences EMT marker protein (N-cadherin, E-cadherin and Vimentin) expression and decreases migration and invasion potential in vivo and in vitro. Mechanistically, L-arabinose induced autophagy and abrogated the nuclear and cytoplasmic expression of β-catenin in BC cells. After adding the Wnt/β-catenin activator LiCl, the efficacy of s on the EMT of BC cells was reversed. Intriguingly, the expression of β-catenin was elevated by the suppression of autophagy using sh-Atg5 lentivirus under L-arabinose treatment. Here, we found L-arabinose contributed to the inhibition of the epithelial–mesenchymal transition (EMT) in breast cancer cells. Moreover, the suppressive effects of L-arabinose on the EMT were regulated by autophagy in BC cells. In addition, we demonstrated that L-arabinose affected the EMT via down-regulating the Wnt/β-catenin signaling pathway, which is dependent on autophagy. Thus, this study provides a novel potential drug for breast cancer therapy.