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L-Selenocysteine induced HepG-2 cells apoptosis through reactive oxygen species-mediated signaling pathway
Kaiying Zhang1, Jingyao Su1, Danyang Chen1
1Center Laboratory, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, 510120, Guangzhou, China.
Background:
Currently, Liver cancer is the fifth most common tumor and the second most important reason for cancer-related death in the world. However, there are still many limitations of the clinical treatment of liver cancer, and new treatment options are clearly needed. Fortunately, studies have shown that L-Selenocysteine has a certain effect on cancer. This study was to investigate the effects of L-Selenocysteine on the inhibition of cell proliferation and the promotion of apoptosis of HepG-2 cells through ROS mediated fine signaling pathway.
Materials And Methods:
CCK-8 assay was applied to evaluating the cytotoxic effect of L-Selenocysteine on HepG-2 cells. Electron microscopy, flow cytometry and Western Blot was utilization in further researching cells signaling pathways.
Results:
The growth of HepG-2 cells was inhibited by L-selenocysteine treatment in a dose-dependent manner. The cell viability decreased to 52.20%, 43.20% and 30.83% under the treatment of 4, 8, 16 µM L-selenocysteine, respectively. L-Selenocysteine had higher cytotoxicity towards HepG-2 cells than normal cells. L-Selenocysteine can induce the apoptosis of HepG-2 cells by increasing the DNA fragmentation, and activating the Caspase-3. In addition, it was found that the mechanism of the induction to HepG-2 cell apoptosis by L-Selenocysteine was closely related to the overproduction of ROS and promoted apoptosis through the Bcl-2 signaling pathway.
Conclusions:
Our data suggest that L-selenocysteine may cause mitochondrial damage and subsequently stimulate ROS production. ROS can damage cellular DNA and mediate the production of Casapase-8, Bid, Bcl-2 and other proteins, affecting downstream signaling pathways, and ultimately induced apoptosis.
Insights
L-Selenocysteine inhibits liver cancer cell growth and promotes apoptosis by increasing reactive oxygen species (ROS) production. This compound shows potential as a novel therapeutic agent for liver cancer treatment.
Area of Science:
- Biochemistry
- Molecular Biology
- Oncology
Background:
- Liver cancer is a leading cause of cancer-related death globally, necessitating novel therapeutic strategies.
- Existing treatments for liver cancer face limitations, highlighting the need for alternative approaches.
- L-Selenocysteine has demonstrated potential anti-cancer properties in preliminary studies.
Purpose of the Study:
- To investigate the anti-proliferative and pro-apoptotic effects of L-Selenocysteine on HepG-2 liver cancer cells.
- To elucidate the role of reactive oxygen species (ROS) in the mechanism of L-Selenocysteine-induced apoptosis.
Main Methods:
- Cytotoxic effects were evaluated using the CCK-8 assay.
- Cellular signaling pathways were analyzed via electron microscopy, flow cytometry, and Western Blotting.
- Apoptosis was assessed by measuring DNA fragmentation and Caspase-3 activation.
Main Results:
- L-Selenocysteine significantly inhibited HepG-2 cell proliferation in a dose-dependent manner.
- L-Selenocysteine exhibited higher cytotoxicity towards HepG-2 cells compared to normal cells.
- Apoptosis induction was linked to increased ROS production, DNA fragmentation, Caspase-3 activation, and modulation of the Bcl-2 signaling pathway.
Conclusions:
- L-Selenocysteine may induce mitochondrial damage, leading to ROS overproduction.
- ROS generated by L-Selenocysteine contribute to DNA damage and apoptosis signaling.
- The findings suggest L-Selenocysteine's potential therapeutic role in liver cancer via ROS-mediated apoptosis.
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