ArticleMolecular biology reports2022
L-Selenocysteine induced HepG-2 cells apoptosis through reactive oxygen species-mediated signaling pathway.
Article in Molecular biology reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- The antisense lncRNA of TAB2 that prevents oxidative stress to enhance the follicular growth in mammals.Communications biology · 2024Article
- Se-methylselenocysteine inhibits inflammatory response in an LPS-stimulated chicken HD11 macrophage-like cell model through the NFKB2 pathway.Frontiers in veterinary science · 2024Article
- Review
- Inhibition of H3N2 Influenza Virus Induced Apoptosis by Selenium Nanoparticles with Chitosan through ROS-Mediated Signaling Pathways.ACS omega · 2023Article
- Selenium-Containing Agents Acting on Cancer-A New Hope?Pharmaceutics · 2022Review
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundCurrently, 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
methodsCCK-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.
resultsThe 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.
conclusionsOur 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.
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Registered trials
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