Endoplasmic Reticulum Stress Signal Mediators Are Targets of Selenium Action

Wu, Yue; Zhang, Haitao; Dong, Yan; Park, Young‐Mee; Ip, Clement

doi:10.1158/0008-5472.can-05-2016

Cited by 100 publications

(109 citation statements)

References 39 publications

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“…Induction of the ER stress response has been reported for such diverse agents as diindolylmethane (DIM), present in cruciferous vegetables, 44 cannabinoids, 45 selenium, 38 arsenic 46 and celecoxib. 25 Lapillonne et al 47 found that the potent synthetic triterpene derivative CDDO also activated expression of stress related genes in MCF7 and MDA-MB-435 human breast cancer cells.…”

Section: Discussionmentioning

confidence: 99%

The growth inhibitory effect of actein on human breast cancer cells is associated with activation of stress response pathways

Einbond

et al. 2007

Intl Journal of Cancer

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Previous studies indicate that the triterpene glycoside actein from the herb black cohosh inhibits growth of human breast cancer cells. This study seeks to identify genes altered in human breast cancer cells by treatment with actein, using gene expression analysis. We treated MDA-MB-453 human breast cancer cells with actein at 2 doses, 20 or 40 lg/mL, for 6 or 24 hr. We identified 5 genes that were activated after each of the treatments that are known to play a role in cellular responses to diverse stresses, including the DNA damage and unfolded protein responses. In addition, four genes that mediate the integrated stress response (ISR), including activating transcription factor 4, were induced under at least one of the 4 treatment conditions. We used hierarchical clustering to define clusters comprising patterns of gene expression. Two ISR genes, activating transcription factor 3 (ATF3) and DNA damage-inducible transcript 3, and lipid biosynthetic genes were activated after exposure to actein at 40 lg/ mL for 6 hr, whereas the cell cycle genes cyclin E2 and cell division cycle 25A were repressed. Our results suggest that actein induces 2 phases of the ISR, the survival phase and the apoptotic phase, depending on the dose and duration of treatment. We confirmed the results of gene expression analysis with real-time RT-PCR for 18 selected genes and Western blot analysis for ATF3. Since actein activated transcription factors that enhance apoptosis, and repressed cell cycle genes, it may be useful in the prevention and therapy of breast cancer. ' 2007 Wiley-Liss, Inc.

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Section: Discussionmentioning

confidence: 99%

The growth inhibitory effect of actein on human breast cancer cells is associated with activation of stress response pathways

Einbond

et al. 2007

Intl Journal of Cancer

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“…37 A monomethylated selenium metabolite, methylselenic acid (MSA), induced ER stress mediators: apoptotic molecules, such as GADD153 and caspase-12 and -7, and survival/rescue molecules, such as phosphorylated ER resident kinase and glucose-regulated protein-78 and -94. Among these, GADD153 is an important transcription factor in apoptosis induction by MSA.…”

Section: Discussionmentioning

confidence: 99%

“…37 Selenium also sensitizes tumor cells to a number of therapeutic drugs and increase the resistance of normal tissues to the toxic effects of these drugs, 38 indicating that selenium may have dual effects: apoptosis response in cancer cells and survival response in normal cells by affecting ER stress mediators. 37 Further investigation on induction of ER stress signals mediators other than GADD153 by combination with EGCG will give us new insights into the molecular mechanisms of cancer 4 -A specific inhibitor of ERK 1/2, PD98059 (PD), and a selective MEK inhibitor, UO126 (UO), both inhibited high expression of GADD153 gene and its protein, and apoptosis induced by cotreatment with EGCG plus celecoxib. SB203580 (SB), a specific inhibitor of p38 MAPK, and calphostin C, a specific inhibitor of protein kinase C, did not.…”

Section: Discussionmentioning

confidence: 99%

Green tea polyphenol stimulates cancer preventive effects of celecoxib in human lung cancer cells by upregulation of GADD153 gene

Suganuma

Kurusu

Suzuki

et al. 2006

Intl Journal of Cancer

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To more clearly understand the molecular mechanisms involved in synergistic enhancement of cancer preventive activity with the green tea polyphenol (2)-epigallocatechin gallate (EGCG), we examined the effects of cotreatment with EGCG plus celecoxib, a cyclooxygenase-2 selective inhibitor. We specifically looked for induction of apoptosis and expression of apoptosis related genes, with emphasis on growth arrest and DNA damage-inducible 153 (GADD153) gene, in human lung cancer cell line PC-9: Cotreatment with EGCG plus celecoxib strongly induced the expression of both GADD153 mRNA level and protein in PC-9 cells, while neither EGCG nor celecoxib alone did. However, cotreatment did not induce expression of other apoptosis related genes, p21 WAF1 and GADD45. Judging by upregulation of GADD153, only cotreatment with EGCG plus celecoxib synergistically induced apoptosis of PC-9 cells. Synergistic effects with the combination were also observed in 2 other lung cancer cell lines, A549 and ChaGo K-1. Furthermore, EGCG did not enhance GADD153 gene expression or apoptosis induction in PC-9 cells in combination with N-(4-hydroxyphenyl)retinamide or with aspirin. Thus, upregulation of GADD153 is closely correlated with synergistic enhancement of apoptosis with EGCG. Cotreatment also activated the mitogen-activated protein kinases (MAPKs), such as ERK1/2 and p38 MAPK: Preteatment with PD98059 (ERK1/2 inhibitor) and UO126 (selective MEK inhibitor) abrogated both upregulation of GADD153 and synergistic induction of apoptosis of PC-9 cells, while SB203580 (p38 MAPK inhibitor) did not do so, indicating that GADD153 expression was mediated through the ERK signaling pathway. These findings indicate that high upregulation of GADD153 is a key requirement for cancer prevention in combination with EGCG. ' 2006 Wiley-Liss, Inc.Key words: EGCG; apoptosis; ERK1/2; prevention (2)-Epigallocatechin gallate (EGCG), a main constituent of green tea polyphenol, can act synergistically with cancer preventive agents (such as sulindac and tamoxifen) in inducing apoptosis of lung, colon and breast cancer cells. 1-3 Since EGCG and green tea have a wide range of target organs and are nontoxic for animals and humans, there is growing interest in increasing the antitumor activity of cancer preventive agents in combination with EGCG or green tea. [4][5][6] However, the molecular mechanisms responsible for the synergistic effects of cotreatment with EGCG plus cancer preventive agents are not known. Using human cDNA cancer expression array, we have found upregulated expressions of 2 genes, growth arrest and DNA damage-inducible gene 153 (GADD153) and p21 WAF1 , and downregulated expressions of 4 genes, T-plasminogen activator, TIMP3, IL-1b and integrin b4: All of these genes are associated with synergistic induction of apoptosis of human non-small-cell lung carcinoma (NSCLC) cell line PC-9 by cotreatment with EGCG plus sulindac. 7 Treatment with either EGCG or sulindac alone did not affect these gene expressions. Since upregulation of GADD153 gene expressi...

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“…The mechanism underlying ER stress-associated apoptosis is poorly understood. It has been proposed recently that caspase-7 could be involved in ER -stress-induced apoptosis through its association with a subpopulation of GRP78 existing as an ER transmembrane protein (Reddy et al, 2003;Rao et al, 2004;Wu et al, 2005). Basically, caspase-7 and GRP78 bind to each other (Wu et al, 2005) preventing the activation of caspase-7 (Reddy et al, 2003).…”

Section: Compared With Cells Incubated For 3 H Cells Incubated With mentioning

confidence: 99%

Relationship between subcellular localisation of Foscan® and caspase activation in photosensitised MCF-7 cells

et al. 2007

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The present study investigates the relationship between the subcellular localisation of Foscan s and intrinsic apoptotic pathway post Foscan s -based photodynamic therapy (PDT). With this purpose, mammary carcinoma MCF-7 cells were incubated with Foscan s for 3 or 24 h and then subjected to equitoxic light doses. Fluorescence microscopy revealed very good Foscan s co-localization to endoplasmic reticulum (ER) and Golgi apparatus after 3 h incubation with MCF-7 cells. Progressive increase in incubation time shows leakage of Foscan s from Golgi apparatus. Twenty-four hours incubation yielded a fluence-dependent enhanced induction of the ERresident glucose-regulated protein 78 (Bip/GRP78), along with a weak mitochondrial damage, thus underscoring the ER as the main site of photodamage after prolonged incubation. Analysis of events implicated in apoptotic pathway after 24 h incubation demonstrated photodamage to Bcl-2 protein in total cellular extract, but not in the mitochondrial fraction. We further determined an increase in caspases-7 and -6 activation, which was strongly related to the expression of GRP78. The above findings demonstrate that Foscan s localisation in ER improves the photoactivation of the caspase-7 apoptotic pathway, which is poorly related to mitochondrial damage.

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Endoplasmic Reticulum Stress Signal Mediators Are Targets of Selenium Action

Abstract: A monomethylated selenium metabolite, called methylseleninic acid (MSA), has recently been shown to cause global thiol redox modification of proteins. These changes represent a form of cellular stress due to protein misfolding or unfolding.

Cited by 100 publications

References 39 publications

The growth inhibitory effect of actein on human breast cancer cells is associated with activation of stress response pathways

The growth inhibitory effect of actein on human breast cancer cells is associated with activation of stress response pathways

Green tea polyphenol stimulates cancer preventive effects of celecoxib in human lung cancer cells by upregulation of GADD153 gene

Relationship between subcellular localisation of Foscan® and caspase activation in photosensitised MCF-7 cells

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