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Selenium induces a multi-targeted cell death process in addition to ROS formation
Marita Wallenberg1, Sougat Misra, Agata M Wasik
1Division of Pathology F46, Department of Laboratory Medicine, Karolinska Institutet, Karolinska University Hospital Huddinge, Stockholm, Sweden.
Journal of Cellular and Molecular Medicine
|January 10, 2014
Summary
Redox-active selenium compounds like selenite, selenodiglutathione, and seleno-DL-cystine induce distinct cell death pathways in HeLa cancer cells. This highlights the potential for species-specific selenium chemotherapeutics to combat cancer drug resistance.
Area of Science:
- Biochemistry
- Cell Biology
- Cancer Research
Background:
- Redox-active selenium compounds show promise as chemotherapeutics due to tumor selectivity and multi-target responses, potentially overcoming drug resistance.
- Selenium's cytotoxic effects on cancer cells involve reactive oxygen species generation and diverse intracellular signaling pathways.
- The specific chemical form of selenium and the cell line influence the mode of cell death induced.
Purpose of the Study:
- To investigate and differentiate the cell death mechanisms induced by three redox-active selenium compounds (selenite, selenodiglutathione, and seleno-DL-cystine) in HeLa cancer cells.
- To elucidate the role of chemical species-specific selenium compounds in cancer cell survival and potential therapeutic applications.
Main Methods:
- Treatment of HeLa cells with varying concentrations of selenite, selenodiglutathione, and seleno-DL-cystine.
- Morphological and molecular analyses to identify distinct cell death phenotypes (apoptosis, necroptosis, paraptosis).
- Assessment of protein thiol glutathionylation and endoplasmic reticulum (ER) stress markers.
Main Results:
- Selenite and selenodiglutathione demonstrated equipotent toxicity (IC50 5 μM) but induced different cell death pathways: necroptosis-like (selenite) and apoptosis-like (selenodiglutathione).
- Selenodiglutathione induced significant glutathionylation of free protein thiols.
- Seleno-DL-cystine (IC50 100 μM) induced two distinct cell death modes: apoptosis-like and paraptosis-like, characterized by ER stress and cytoplasmic vacuolation.
Conclusions:
- The study reveals diverse cytotoxic effects and cell death mechanisms of different redox-active selenium compounds in HeLa cells.
- Findings underscore the potential for tailored, chemical species-specific selenium therapies in cancer treatment.
- Understanding these distinct pathways is crucial for developing effective selenium-based anticancer strategies and preventing drug resistance.
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