Ginsenoside Rg3 promotes cytotoxicity of Paclitaxel through inhibiting NF-κB signaling and regulating Bax/Bcl-2 expression on triple-negative breast cancer.

Abstract

Taxane-based chemotherapy regimen is the most effective therapeutic strategy for triple-negative breast cancer (TNBC) which is an aggressive subtype of breast cancer with high rate of recurrence and distant metastasis. Ginsenoside Rg3 is isolated from Panax ginseng with anti-cancer activity against carcinomas. We aim to evaluate the chemosensitizing effects of Ginsenoside Rg3 on TNBC cells and xenograft and explore the underlying mechanism. Human triple-negative breast cancer lines MDA-MB-231, MDA-MB-453 and BT-549 were used. Cell viability and survival was detected by MTT assay and colony formation assay. Apoptosis was detected by Annexin V/PI assay and TUNEL. Enzyme-linked immunosorbent assay was performed to determine NF-κB activation. The NF-κB p65, Bcl 2, Bax and Caspase-3 protein expression were detected using Western blot analysis. The results showed that Ginsenoside Rg3 promotes cytotoxicity and apoptosis of Paclitaxel on TNBC cell lines and xenograft. Ginsenoside Rg3 combined Paclitaxel inhibited NF-κB activation, decreased NF-κB p65 and Bcl-2 protein expressions, increased Bax and Caspase-3 protein expressions. The ratio of Bax/Bcl-2 was significantly enhanced by the Ginsenoside Rg3 to Paclitaxel. Ginsenoside Rg3 promotes cytotoxicity and apoptosis of Paclitaxel by inhibiting NF-κB signaling and modulating Bax/Bcl-2 expression on TNBC. Ginsenoside Rg3 should be regarded as a good chemosensitizing agent for TNBC treatment.