Article Publish Status: FREE
Abstract Title:

Diosgenin‑induced autophagy and apoptosis in a human prostate cancer cell line.

Abstract Source:

Mol Med Rep. 2016 Nov ;14(5):4349-4359. Epub 2016 Sep 19. PMID: 27667394

Abstract Author(s):

Chao Nie, Jie Zhou, Xiaokang Qin, Xianming Shi, Qingqi Zeng, Jia Liu, Shihai Yan, Lei Zhang

Article Affiliation:

Chao Nie


Diosgenin, a plant steroid compound from Dioscorea nipponica, is an anti-inflammatory, antidiabetic, antitumor, vasodilatory compound, which also reduces blood lipid content and protects against ischemia‑induced neuronal damage. However, a limited number of studies have been performed on the antitumor effect of diosgenin on prostate cancer, the underlying mechanism of which remains to be fully elucidated. In the present study, the effect and underlying mechanism of diosgenin on DU145 human prostate cancer cells was investigated. DU145 cells were cultured in vitro with diosgenin, following which cell proliferation was detected by a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and apoptosis was detected by flow cytometry. In addition, DU145 cells were observed under a transmission electron microscope to confirm autophagy. monodansylcadaverine staining and western blotting indicated the levels of autophagy in DU145 cells. To determine the mechanism underlying the effect of diosgenin on DU145 cells, western blotting was performed to evaluate the involvement of the phosphatidylinositol 3 kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) signaling pathway. To investigate the association between apoptosis and autophagy, DU145 cells were cultured with diosgenin and 3‑methyladenine. Hoechst 33342/propidium iodide double staining was performed to detect apoptosis, and reverse transcription‑quantitative polymerase chain reaction was used to analyze mRNA expression levels of Beclin 1 and B‑cell lymphoma 2. Diosgenin inhibits the proliferation of DU145 cells by activating apoptosis and autophagy, and the mechanism underlying this activation may be associated with the inhibition of the PI3K/Akt/mTOR signaling pathway. In addition, the inhibition of autophagy mediated by diosgenin increases apoptosis and, thus, increases the therapeutic effect. The combination of diosgenin with an autophagy inhibitor may be an effective strategyto increase the antitumor effect of diosgenin.

Study Type : In Vitro Study

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