Dioscin strengthens the efficiency of adriamycin in MCF-7 and MCF-7/ADR cells through autophagy induction: More than just down-regulation of MDR1 | Zendy

Changyuan Wang | Zendy; Xiaokui Huo | Zendy; Lijuan Wang | Zendy; Qiang Meng | Zendy; Zhihao Liu | Zendy; Qi Liu | Zendy; Huijun Sun | Zendy; Pengyuan Sun | Zendy; Jinyong Peng | Zendy; Kexin Liu | Zendy

Open Access

Dioscin strengthens the efficiency of adriamycin in MCF-7 and MCF-7/ADR cells through autophagy induction: More than just down-regulation of MDR1

Author(s) -

Changyuan Wang,

Xiaokui Huo,

Lijuan Wang,

Qiang Meng,

Zhihao Liu,

Qi Liu,

Huijun Sun,

Pengyuan Sun,

Jinyong Peng,

Kexin Liu

Publication year - 2016

Publication title -

scientific reports

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.24

H-Index - 213

ISSN - 2045-2322

DOI - 10.1038/srep28403

Subject(s) - autophagy , mcf 7 , downregulation and upregulation , protein kinase b , pi3k/akt/mtor pathway , cytotoxicity , chemistry , cancer research , phosphorylation , pharmacology , doxorubicin , cell growth , cell culture , cancer cell , signal transduction , apoptosis , medicine , biology , in vitro , cancer , biochemistry , chemotherapy , gene , human breast , genetics

The purpose of present study was to investigate the effect of dioscin on activity of adriamycin (ADR) in ADR-sensitive (MCF-7) and ADR-resistant (MCF-7/ADR) human breast cancer cells and to clarify the molecular mechanisms involved. Antiproliferation effect of ADR was enhanced by dioscin in MCF-7 and MCF-7/ADR cells. Dioscin significantly inhibited MDR1 mRNA and protein expression and MDR1 promoter and nuclear factor κ-B (NF-κB) activity in MCF-7/ADR cells. Additionally, inhibitor κB-α (IκB-α) degradation was inhibited by dioscin. Moreover, dioscin induced the formation of vacuoles in the cytoplasm and protein level of LC3-II in MCF-7 and MCF-7/ADR cells. Autophagy inhibitor 3-MA abolished the effect of dioscin on ADR cytotoxicity. Dioscin inhibited phosphorylation of PI3K and Akt, resulting in upregulation of LC3-II expression. In conclusion, dioscin increased ADR chemosensitivity by down-regulating MDR1 expression through NF-κB signaling inhibition in MCF-7/ADR cells. Autophagy was induced by dioscin to ameliorate the cytotoxicity of ADR via inhibition of the PI3K/AKT pathways in MCF-7 and MCF-7/ADR cells. These findings provide evidence in support of further investigation into the clinical application of dioscin as a chemotherapy adjuvant.

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