Breast cancer is a common malignancy that is highly lethal. Due to the poor prognosis, more effective and efficient treatment methods are urgently needed. Rutin (RUT) is a traditional Chinese medicine reported to have a variety of pharmacological properties, including anticancer properties. However, the effects of RUT on breast cancer and its underlying molecular mechanism of action remain unclear. In the present study, we observed a significant downregulation of microRNA (miR)-129-1-3p in mouse breast cancer cells (4T1) compared with the expression in mouse normal breast epithelial cells (HC11). We also found that RUT could increase the expression of miR-129-1-3p in 4T1 cells and suppress cell proliferation. To elucidate the molecular mechanism of action of RUT, miR-129-1-3p mimics and its inhibitor were transfected into 4T1 cells. miR-129-1-3p overexpression could inhibit the proliferation, invasion, migration, and calcium overload of mouse breast cancer cells and also enhance apoptosis, whereas miR-129-1-3p knockdown had the opposite effects. Taken together, cell-based experiments indicated that RUT restrains the growth of mouse breast cancer cells by regulating the miR-129-1-3p/Ca2+ signaling pathway. This study also revealed the inhibitory effect of RUT on breast cancer cells at the noncoding RNA level and provided a theoretical foundation for the application of RUT as a drug to inhibit tumor growth.
Keywords: Ca2+ signaling pathway; Rutin; breast cancer; miR-129-1-3p; proliferation.
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