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Breast cancer (BC) is one of the most common malignant tumor, the incidence of which has increased worldwide in recent years. Ginsenosides are the main active components of Panax ginseng C. A. Mey., in vitro and in vivo studies have confirmed that ginsenosides have significant anti-cancer activity, including BC. It is reported that ginsenosides can induce BC cells apoptosis, inhibit BC cells proliferation, migration, invasion, as well as autophagy and angiogenesis, thereby suppress the procession of BC. In this review, the therapeutic effects and the molecular mechanisms of ginsenosides on BC will be summarized. And the combination strategy of ginsenosides with other drugs on BC will also be discussed. In addition, epigenetic changes, especially microRNAs (miRNAs) targeted by ginsenosides in the treatment of BC are clarified.

Fourteen compounds were isolated from Pueraria lobata (Willd.) Ohwi by column chromatography and preparative thin-layer chromatography; the structures were identified by spectroscopic analysis and compared with data reported in the literature. Seven compounds were isolated and identified from Pueraria lobata for the first time: Linoleic acid, Sandwicensin, Isovanillin, Ethyl ferulate, Haginin A, Isopterofuran, 3′.7-Dihydroxyisoflavan. The other 10 compounds were structurally identified as follows: Lupenone, Lupeol, β-sitosterol, Genistein, Medicarpin, Coniferyl Aldehyde, Syringaldehyde. All compounds were evaluated for their ability to inhibit SW480 and SW620 cells using the CCK-8 method; compound 5 (Sandwicensin) had the best activity, and compounds 6, 9, 11 and 12 exhibited moderate inhibitory activity. In addition, the targets and signaling pathways of Sandwicensin treatment for CRC were mined using network pharmacology, and MAPK3, MTOR, CCND1 and CDK4 were found to be closely associated with Sandwicensin treatment for CRC; the GO and KEGG analysis showed that Sandwicensin may directly regulate the cycle, proliferation and apoptosis of CRC cells through cancer-related pathways.