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Published on: July 17, 2018
Aesculetin-induced apoptosis through a ROS-mediated mitochondrial dysfunction pathway in human cervical cancer cells
Jin Yang1, Yu-Ling Xiao, Xian-Ran He
1State Key Laboratory of Virology, College of Pharmacy, Wuhan University, Wuhan, China.
Abstract:
Aesculetin (1) is an important coumarin found in various plant materials. It has been shown to have antiproliferative effects on several types of human cancer cells, but its effect on cervical cancer cells in vitro is unknown. In this study, we investigated that the cytotoxic effect of 1 on a non-cancer cell line (293) was smaller than on a tumor cell line (HeLa). This is the first report showing the possible mechanism of antiproliferative effect of 1 for the prevention of cervical cancer in cell culture models. It was found that 1 inhibited cell viability by inducing apoptosis, as evidenced by the formation of apoptotic bodies, generation of reactive oxygen species (ROS), and the accumulation of cells in the sub-G1 phase. Treatment with compound 1 decreased the cell growth in a dose-dependent manner with an IC(50) value of 37.8 microM. Aesculetin-induced apoptosis was correlated with mitochondrial dysfunction (DeltaPsi(m)), leading to the release of cytochrome c from the mitochondria to the cytosol, as well as the proteolytic activation of caspases in HeLa cells. These results indicate that 1 induces apoptosis in HeLa cells through a ROS-mediated mitochondrial dysfunction pathway.
Insights
Aesculetin exhibits antiproliferative effects against cervical cancer cells by inducing apoptosis. This compound triggers cell death through reactive oxygen species generation and mitochondrial dysfunction in HeLa cells.
Area of Science:
- Pharmacology
- Cell Biology
- Biochemistry
Background:
- Aesculetin is a coumarin with known antiproliferative properties.
- Its effects on cervical cancer cells remain largely uncharacterized.
- This study explores the mechanism of aesculetin's action on cervical cancer.
Purpose of the Study:
- To investigate the cytotoxic effects of aesculetin on cervical cancer cells (HeLa).
- To elucidate the underlying mechanism of aesculetin-induced antiproliferation.
- To assess the potential of aesculetin for cervical cancer prevention.
Main Methods:
- Cell viability assays on HeLa and 293 cell lines.
- Analysis of apoptosis markers including apoptotic bodies and sub-G1 phase accumulation.
- Measurement of reactive oxygen species (ROS) generation.
- Assessment of mitochondrial membrane potential (ΔΨm) and cytochrome c release.
- Evaluation of caspase activation.
Main Results:
- Aesculetin demonstrated greater cytotoxicity towards HeLa cells compared to non-cancerous 293 cells.
- Cell viability decreased in a dose-dependent manner with an IC50 of 37.8 μM.
- Aesculetin induced apoptosis via ROS generation, mitochondrial dysfunction, and caspase activation.
- Mitochondrial dysfunction led to cytochrome c release and subsequent apoptosis.
Conclusions:
- Aesculetin effectively inhibits cervical cancer cell growth by inducing apoptosis.
- The mechanism involves a reactive oxygen species-mediated mitochondrial pathway.
- Aesculetin shows potential as a therapeutic agent for cervical cancer prevention.
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