Modulation of redox status in human lung cell lines by organoselenocompounds: Selenazolidines, selenomethionine, and methylseleninic acid

Poerschke, Robyn L.; Franklin, Michael R.; Moos, Philip J.

doi:10.1016/j.tiv.2008.08.003

Cited by 33 publications

(37 citation statements)

References 37 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The results show that 1.3 μM MSA caused a significant decrease in the levels of ROS at 24 and 48 h (Figure 7). This decrease is consistent with the increased cellular free thiol levels observed by Poerschke et al [60] after 24 h MSA incubation. Cells incubated with MSA for 72 h had similar ROS level to control cells.…”

Section: Resultssupporting

confidence: 92%

Methylseleninic acid promotes antitumour effects via nuclear FOXO3a translocation through Akt inhibition

Tarrado‐Castellarnau

Cortés

Zanuy

et al. 2015

Pharmacological Research

View full text Add to dashboard Cite

Selenium supplement has been shown in clinical trials to reduce the risk of different cancers including lung carcinoma. Previous studies reported that the antiproliferative and pro-apoptotic activities of methylseleninic acid (MSA) in cancer cells could be mediated by inhibition of the PI3K pathway. A better understanding of the downstream cellular targets of MSA will provide information on its mechanism of action and will help to optimise its use in combination therapies with PI3K inhibitors. For this study, the effects of MSA on viability, cell cycle, metabolism, apoptosis, protein and mRNA expression, and Reactive Oxygen Species production were analysed in A549 cells. FOXO3a subcellular localisation was examined in A549 cells and in stably transfected human osteosarcoma U2foxRELOC cells. Our results demonstrate that MSA induces FOXO3a nuclear translocation in A549 cells and in U2OS cells that stably express GFP-FOXO3a. Interestingly, sodium selenite, another selenium compound, did not induce any significant effects on FOXO3a translocation despite inducing apoptosis. Single strand break of DNA, disruption of tumour cell metabolic adaptations, decrease in ROS production, and cell cycle arrest in G1 accompanied by induction of apoptosis are late events occurring after 24 h of MSA treatment in A549 cells. Our findings suggest that FOXO3a is a relevant mediator of the antiproliferative effects of MSA. This new evidence on the mechanistic action of MSA can open new avenues in exploiting its antitumour properties and in the optimal design of novel combination therapies. We present MSA as a promising chemotherapeutic agent with synergistic antiproliferative effects with cisplatin.

show abstract

Section: Resultssupporting

confidence: 92%

Methylseleninic acid promotes antitumour effects via nuclear FOXO3a translocation through Akt inhibition

Tarrado‐Castellarnau

Cortés

Zanuy

et al. 2015

Pharmacological Research

View full text Add to dashboard Cite

show abstract

“…Thus, MSeA acts as a prooxidant to promote cell dysfunction and death. More recently, MSeA treatment (2.5-5 lM) was found to significantly increase thiol concentration and oxidative stress in the endoplasmic reticulum of human lung carcinoma cells [261]. In addition, MSeA has been found to decrease expression of several kinases involved in cell growth and apoptotic pathways [262], particularly protein kinase C [263], at low micromolar concentrations.…”

Section: Oxo-selenium Compoundsmentioning

confidence: 99%

Antioxidant and Anticancer Properties and Mechanisms of Inorganic Selenium, Oxo-Sulfur, and Oxo-Selenium Compounds

Ramoutar

Brumaghim

2010

Cell Biochem Biophys

102

View full text Add to dashboard Cite

Inorganic selenium and oxo-sulfur compounds are widely available in dietary supplements and have been extensively studied for their antioxidant and anticancer properties. Although many in vivo and clinical trials have been conducted using these compounds, their biochemical and chemical mechanisms of efficacy are the focus of much current research. This review discusses the ability of inorganic selenium compounds, such as selenite, and selenate, to prevent damage from reactive oxygen species as well as their ability to promote cell death by reactive oxygen species generation. Oxo-sulfur and selenium compounds, such as allicin, dimethyl sulfone, methionine sulfoxide, and methylselenenic acid also have similar abilities to act as both antioxidants and pro-oxidants, but the mechanisms for these behaviors are distinctly different from those of the inorganic selenium compounds. The antioxidant and pro-oxidant properties of these small-molecule sulfur and selenium compounds are extremely complex and often greatly depend on experimental conditions, which may explain contradictory literature reports of their efficacy.

show abstract

“…Studies have shown that low doses of selenium are helpful for cancer prevention because of its antioxidant effects, and moderate to high doses of selenium are helpful for cancer therapy because of the prooxidant effects [24]. Of note, the oxidative stress in cancer cells induced by selenium is significantly attenuated in normal cells [25]. It has been reported that the toxic concentration of selenium in hepatocytes is at least ten times higher than that in cancer cells.…”

Section: Discussionmentioning

confidence: 99%

Protective Role of Selenium Compounds on the Proliferation, Apoptosis, and Angiogenesis of a Canine Breast Cancer Cell Line

Liu

Guo

et al. 2015

Biol Trace Elem Res

View full text Add to dashboard Cite

We herein examined the effects of different doses, forms, and compatibilities of selenium on a canine mammary gland tumor cell line, CTM1211, and explored the related mechanisms. Three selenium compounds, sodium selenite (SSE), methylseleninic acid (MSA), and methylselenocysteine (MSC), were selected for these experiments, and cyclophosphamide (CTX) served as a positive control. In the cell viability assay, the cell viability of each group at 48/72 h decreased significantly compared with the control group (p < 0.05), and the cell viability of the CTX + MSA group was lower than that of CTX and MSA groups (p < 0.05). Moreover, the inhibitory effect of selenium on cell proliferation was time-dependent but not concentration-dependent. In the cell apoptosis assay, the apoptosis values of each group increased significantly compared with the control group, and the apoptosis values of the CTX + MSA group increased the most significantly (p < 0.01). The protein and mRNA expression levels of vascular endothelial growth factor-alpha (VEGF-alpha), angiopoietin-2 (Ang-2), and hypoxia inducible factor-1 alpha (HIF-1 alpha) were downregulated in each group, while that of phosphatase and tensin homolog (PTEN) were upregulated (p < 0.05). In conclusion, these three selenium compounds, especially MSA, could significantly inhibit the viability and growth of the CTM1211 cell line, which is partly due to the induction of apoptosis and regulation of tumor angiogenesis.

show abstract

Modulation of redox status in human lung cell lines by organoselenocompounds: Selenazolidines, selenomethionine, and methylseleninic acid

Cited by 33 publications

References 37 publications

Methylseleninic acid promotes antitumour effects via nuclear FOXO3a translocation through Akt inhibition

Methylseleninic acid promotes antitumour effects via nuclear FOXO3a translocation through Akt inhibition

Antioxidant and Anticancer Properties and Mechanisms of Inorganic Selenium, Oxo-Sulfur, and Oxo-Selenium Compounds

Protective Role of Selenium Compounds on the Proliferation, Apoptosis, and Angiogenesis of a Canine Breast Cancer Cell Line

Contact Info

Product

Resources

About