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Novel Strategy in Breast Cancer Therapy: Revealing The Bright Side of Ginsenosides

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CURRENT MOLECULAR PHARMACOLOGY
卷 14, 期 6, 页码 1093-1111

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BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/1874467214666210120153348

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Breast cancer; ginsenoside; apoptosis; cancer therapy; MicroRNA; autophagy

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Ginsenosides exhibit anti-tumor activity against breast cancer cells by inducing apoptosis and cell cycle arrest, inhibiting epithelial-to-mesenchymal transition, matrix metalloproteinase proteins and angiogenesis, and enhancing chemotherapy efficacy by suppressing migration and proliferation.
Breast cancer is one of the leading causes of death worldwide. Breast cancer cells demonstrate uncontrolled proliferation and high metastatic capacity. They can obtain resistance to chemotherapy and radiotherapy. This has resulted in troublesome treatment of breast cancer. Nature as a rich source of plant derived-natural products with anti-tumor activity can be of interest in breast cancer therapy. Ginsenosides are triterpenoid saponins and considered as secondary metabolites exclusively found in Panax species. From immemorial times, ginsenosides have been applied in the treatment of various disorders such as diabetes, inflammatory diseases, neurological disorders, and particularly, cancer. In the present review, we highlight the anti-tumor activity of ginsenosides against breast cancer cells. Ginsenosides are able to induce apoptosis and cell cycle arrest. They interfere with breast cancer metastasis via inhibiting epithelial-to-mesenchymal transition, matrix metalloproteinase proteins and angiogenesis. Ginsenosides can promote the efficacy of chemotherapy via suppressing migration and proliferation. Molecular pathways such as phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt), insulin-like growth factor-1, Wnt, microRNAs and long non-coding RNAs are affected by ginsenosides in suppressing breast cancer malignancy. Consequently, ginsenosides are versatile compounds in breast cancer therapy by suppressing the growth and invasion, as well as promoting their sensitivity to chemotherapy.

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