Autophagy inhibition enhances apoptosis induced by dioscin in huh7 cells
Ming-Ju Hsieh1, Shun-Fa Yang, Yih-Shou Hsieh
1School of Medical Laboratory and Biotechnology, Chung Shan Medical University, 110, Section 1, Chien-Kuo N. Road, Taichung 402, Taiwan.
Abstract:
Extensive research results support the application of herbal medicine or natural food as an augment during therapy for various cancers. However, the effect of dioscin on tumor cells autophagy has not been clearly clarified. In this study, the unique effects of dioscin on autophagy of hepatoma cells were investigated. Results found that dioscin induced caspase-3- and -9-dependent cell apoptosis in a dose-dependent manner. Moreover, inhibition of ERK1/2 phosphorylation significantly abolished the dioscin-induced apoptosis. In addition, dioscin triggered cell autophagy in early stages. With autophagy inhibitors to hinder the autophagy process, dioscin-induced cell apoptosis was significantly enhanced. An inhibition of caspase activation did not affect the dioscin-induced LC3-II protein expression. Based on the results, we believed that while apoptosis was blocked, dioscin-induced autophagy process also diminished in Huh7 cells. In conclusion, this study indicates that dioscin causes autophagy in Huh7 cells and suggests that dioscin has a cytoprotective effect.
Insights
Dioscin induces autophagy in hepatoma cells, a process that appears cytoprotective. Inhibiting autophagy enhances dioscin-induced apoptosis, suggesting a complex role in cancer therapy.
Area of Science:
- Cell Biology
- Cancer Research
- Pharmacology
Background:
- Herbal medicines show promise as adjunct cancer therapies.
- The specific impact of dioscin on tumor cell autophagy remains unclear.
- Hepatoma cells are a key focus for cancer treatment research.
Purpose of the Study:
- To investigate the effects of dioscin on hepatoma cell autophagy.
- To elucidate the relationship between dioscin, apoptosis, and autophagy.
- To determine dioscin's potential cytoprotective role in hepatoma cells.
Main Methods:
- Dose-dependent treatment of Huh7 hepatoma cells with dioscin.
- Assessment of apoptosis via caspase-3 and caspase-9 activation.
- Analysis of autophagy markers, including LC3-II protein expression.
- Utilized ERK1/2 phosphorylation inhibition and autophagy inhibitors.
Main Results:
- Dioscin induced dose-dependent apoptosis, dependent on caspase-3 and -9 activation.
- Inhibition of ERK1/2 phosphorylation blocked dioscin-induced apoptosis.
- Dioscin triggered autophagy in early stages, with increased LC3-II expression.
- Autophagy inhibition enhanced dioscin-induced apoptosis, while blocking apoptosis diminished autophagy.
Conclusions:
- Dioscin induces autophagy in Huh7 hepatoma cells.
- Dioscin exhibits a cytoprotective effect, potentially mediated by autophagy.
- The interplay between apoptosis and autophagy is crucial in dioscin's action.
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