Comparative proteomic analysis of apoptosis induced by sodium selenite in human acute promyelocytic leukemia NB4 cells

Dong, Hua; Ying, Tianyi; Li, Ting; Cao, Tingming; Wang, Junjun; Yuan, Jing; Feng, Erling; Han, Bingshe; Hua, Fangyuan; Yang, Yang; Yuan, Jing; Wang, Hengliang; Xu, Caimin

doi:10.1002/jcb.20755

Cited by 20 publications

(12 citation statements)

References 32 publications

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“…Comparative 2D gel electrophoresis of sodium selenite-induced apoptosis in human leukemia NB4 cells has been performed and confirmed by RT-PCR and Western blot (Dong et al 2006). Out of the 26 downregulated and four upregulated proteins that exhibited a minimum 1.5 fold change in that study, only a-tubulin, b-actin and LAMR1 were also identified in our CHO IgG-9b8 study.…”

Section: Discussionmentioning

confidence: 55%

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Proteomics analysis of chinese hamster ovary cells undergoing apoptosis during prolonged cultivation

et al. 2011

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The degradation of environmental conditions, such as nutrient depletion and accumulation of toxic waste products over time, often lead to premature apoptotic cell death in mammalian cell cultures and suboptimal protein yield. Although apoptosis has been extensively researched, the changes in the whole cell proteome during prolonged cultivation, where apoptosis is a major mode of cell death, have not been examined. To our knowledge, the work presented here is the first whole cell proteome analysis of non-induced apoptosis in mammalian cells. Flow cytometry analyses of various activated caspases demonstrated the onset of apoptosis in Chinese hamster ovary cells during prolonged cultivation was primarily through the intrinsic pathway. Differential in gel electrophoresis proteomic study comparing protein samples collected during cultivation resulted in the identification of 40 differentially expressed proteins, including four cytoskeletal proteins, ten chaperone and folding proteins, seven metabolic enzymes and seven other proteins of varied functions. The induction of seven ER chaperones and foldases is a solid indication of the onset of the unfolded protein response, which is triggered by cellular and ER stresses, many of which occur during prolonged batch cultures. In addition, the upregulation of six glycolytic enzymes and another metabolic protein emphasizes that a change in the energy metabolism likely occurred as culture conditions degraded and apoptosis advanced. By identifying the intracellular changes during cultivation, this study provides a foundation for optimizing cell line-specific cultivation processes, prolonging longevity and maximizing protein production.

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Section: Discussionmentioning

confidence: 55%

“…Induced apoptosis has been studied in various cell lines using a number of approaches (Baik and Lee 2010;Dong et al 2006;Schmidt et al 2007;Thiede et al 2006). Comparative 2D gel electrophoresis of sodium selenite-induced apoptosis in human leukemia NB4 cells has been performed and confirmed by RT-PCR and Western blot (Dong et al 2006).…”

Section: Discussionmentioning

confidence: 99%

Proteomics analysis of chinese hamster ovary cells undergoing apoptosis during prolonged cultivation

et al. 2011

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“…The specific activation of p38 and JNK in cells exposed to various selenium compounds has been reported by several authors (Ghose et al 2001;Jiang et al 2004a, b;Kim et al 2004;Dong et al 2006). On the other hand, ebselen and selenite have been shown to inhibit p38 and JNK pathways by thiol-redox mechanism (Park et al 2000;Sarker et al 2003).…”

Section: Discussionmentioning

confidence: 82%

Selenium activates p53 and p38 pathways and induces caspase-independent cell death in cervical cancer cells

Rudolf

Červinka

2007

Cell Biol Toxicol

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The mechanisms of sodium selenite-induced cell death in cervical carcinoma cells were studied during 24 h of exposure in the HeLa Hep-2 cell line. Selenite at the employed concentrations of 5 and 50 micromol/L produced time- and dose-dependent suppression of DNA synthesis and induced DNA damage which resulted in phosphorylation of histone H2A.X. These effects were influenced by pretreatment of cells with the SOD/catalase mimetic MnTMPyP or glutathione-depleting buthionine sulfoximine, suggesting the significant role of selenite-generated oxidative stress. Following the DNA damage, selenite activated p53-dependent pathway as evidenced by the appearance of phosphorylated p53 and accumulation of p21 in the treated cells. Concomitantly, selenite activated p38 pathway but its effect on JNK was very weak. p53- and p38-dependent signaling led to the accumulation of Bax protein, which was preventable by specific inhibitors of p38 (SB 203580) and p53 (Pifithrin-alpha). Mitochondria in selenite-treated cells changed their dynamics (shape and localization) and released AIF and Smac/Diablo, which initiated caspase-independent apoptosis as confirmed by the caspase-3 activity assay and the low effect of caspase inhibitors z-DEVD-fmk and z-VAD-fmk on cell death. We conclude that selenite induces caspase-independent apoptosis in cervical carcinoma cells mostly by oxidative stress-mediated activation of p53 and p38 pathways, but other selenite-mediated effects, in particular mitochondria-specific ones, are also involved.

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“…In acute promyelocytic leukemia (APL) this compound induced apoptosis [180]. The kinases that are modulated by sodium selenite include the MAPK family, serine threonine kinase receptor-associated protein (UNRIP), c-Myc, c-Jun and cFos.…”

Section: Methylseleninic Acid and Sodium Selenitementioning

confidence: 99%

Kinase Regulation by Sulfur and Selenium Containing Compounds

Sanmartín

Plano²,

Font³

et al. 2011

CCDT

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Kinases are enzymes that are involved in a wide-range of cellular targets such as cell proliferation, metabolism, survival and apoptosis. Aberrations in the activity of the kinases have been linked to many human diseases such as diabetes, inflammation and cancer. The discovery of more than 518 kinases encoded by the human genome has spurred the development of rapid screening techniques for potential drugs against these enzymes and these have been identified as interesting targets for medicinal chemistry programs, especially in cancer therapy. On the other hand, sulfur and selenium have been increasingly recognized as essential elements in biology and medicine. Converging data from epidemiological and clinical studies have highlighted these elements as effective chemopreventive agents, particularly against various types of cancer (prostate, lung, breast, leukemia, colon, skin, lymphome, thyroid, pancreas, liver). These elements act through a wide range of potential mechanisms where one identified signal pathway event is kinase modulation, which is common for the two elements and emerges as a valid target. The kinases modulated by sulfur and selenium derivatives include MAP, ERK, JNK, Akt, Cdc2, Cyclin B1 and Cdc25c amongst others. Although both of the elements in question are in the same group in the periodic table and have similar biochemistries, there are relevant differences related to redox potentials, stabilities, oxidation states and anticancer activity. Literature data suggest that the replacement of sulfur by selenium in established cancer chemopreventive agents results in more effective chemopreventive analogs. In view of the multi-target kinase mechanisms in preventing cellular transformation, as well as the differences and similarities between them, in this review we focus on the development of new structures that contain selenium and/or sulfur and discuss our understanding of the regulation of antitumoral effects with emphasis on kinase modulation activity and its implications in cancer.

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Comparative proteomic analysis of apoptosis induced by sodium selenite in human acute promyelocytic leukemia NB4 cells

Cited by 20 publications

References 32 publications

Proteomics analysis of chinese hamster ovary cells undergoing apoptosis during prolonged cultivation

Proteomics analysis of chinese hamster ovary cells undergoing apoptosis during prolonged cultivation

Selenium activates p53 and p38 pathways and induces caspase-independent cell death in cervical cancer cells

Kinase Regulation by Sulfur and Selenium Containing Compounds

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