Abstract
Selenium (Se) is an essential trace element involved in different physiological functions of the human body and plays a role in cancer prevention and treatment. Induction of apoptosis is considered an important cellular event that can account for the cancer preventive effects of Se. The mechanisms of Se-induced apoptosis are associated with the chemical forms of Se and their metabolism as well as the type of cancer studied. So, some selenocompounds, such as SeO2 involve the activation of caspase-3 while sodium selenite induces apoptosis in the absence of the activation of caspases. Modulation of mitochondrial functions has been reported to play a key role in the regulation of apoptosis and also to be one of the targets of Se compounds. Other mechanisms for apoptosis induction are the modulation of glutathione and reactive oxygen species levels, which may function as intracellular messengers to regulate signaling pathways, or the regulation of kinase, among others. Emerging evidence indicates the overlaps between the apoptosis and other types of cell death such as autophagy. In this review we report different processes of cell death induced by Se compounds in cancer treatment and prevention.
Highlights
Selenium (Se) is an oligoelement with essential biological functions and belongs to the most extensively studied chemopreventive compounds [1,2]
There are emerging evidences that cell death caused by Se and Se compounds can occur by apoptotic pathway but can proceed by non-apoptotic modes such as autophagy, necrosis, mitotic catastrophe or combinations thereof, because there are overlaps among them [21]
Recent reports have shown that Se compounds are able to induce tumor cell apoptosis through distinct mechanisms according to cell type and compound pattern
Summary
Selenium (Se) is an oligoelement with essential biological functions and belongs to the most extensively studied chemopreventive compounds [1,2]. There are emerging evidences that cell death caused by Se and Se compounds can occur by apoptotic pathway but can proceed by non-apoptotic modes such as autophagy, necrosis, mitotic catastrophe or combinations thereof, because there are overlaps among them [21]. This has been demonstrated in NB4 cells treated with sodium selenite that suppressed autophagy and increased apoptosis through phosphoinositide-3-kinase (PI3K)/Akt [22]. Sodium selenite (Na2SeO3); Methylseleninic acid (MSA); Selenous acid; Selenium dioxide (SeO2)
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