Enhanced selenium effect on growth arrest by BiP/GRP78 knockdown in p53-null human prostate cancer cells

K, Zu; Bihani, Teeru; Ao, Lin; Ym, Park; Mori, Kazutoshi; C, Ip

doi:10.1038/sj.onc.1209071

Cited by 95 publications

(85 citation statements)

References 49 publications

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“…The activity of calcineurin is dependent on calcium, and MSA enhances calcium release from the endoplasmic reticulum. Presently, we are also investigating the signals emanating from endoplasmic reticulum stress as molecular switches turned on by MSA in facilitating a commitment to apoptosis (23,24). The mechanisms of endoplasmic reticulum stress -associated apoptosis include a direct release of caspases from the endoplasmic reticulum, as well as an indirect activation of both the intrinsic (mitochondrial) and extrinsic (death receptor-mediated) pathways.…”

Section: Discussionmentioning

confidence: 99%

Selenium sensitizes MCF-7 breast cancer cells to doxorubicin-induced apoptosis through modulation of phospho-Akt and its downstream substrates

Li¹,

Zhou

Wang

et al. 2007

Molecular Cancer Therapeutics

109

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Section: Discussionmentioning

confidence: 99%

Selenium sensitizes MCF-7 breast cancer cells to doxorubicin-induced apoptosis through modulation of phospho-Akt and its downstream substrates

Li¹,

Zhou

Wang

et al. 2007

Molecular Cancer Therapeutics

109

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“…Based on a rapid suppression of vascular endothelial growth factor, matrix metalloproteinase-2, and prostate-specific antigen by MSeA in different cell model systems and their common characteristic of being secretory proteins with disulfide bonds, we have speculated that MSeA could induce unfolded protein response in the ER to lead to their rapid protein degradation (11). Ip and coworkers (48) have shown that PC-3 cells exposed to MSeA in cell culture display ER stress responses including GRP78 and CHOP (Oncovin)/gadd153. Taken together, these findings suggest that MSeA may specifically restore ER stress rescue and chaperone-like proteins in the prostate epithelial cells to contribute to the inhibition of carcinogenesis.…”

Section: Discussionmentioning

confidence: 99%

Proteomic Profiling of Potential Molecular Targets of Methyl-Selenium Compounds in the Transgenic Adenocarcinoma of Mouse Prostate Model

Zhang

Wang

Anderson

et al. 2010

Cancer Prevention Research

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Because the Selenium (Se) and Vitamin E Cancer Prevention Trial (SELECT) failed to show the efficacy of selenomethionine for prostate cancer prevention, there is a critical need to identify safe and efficacious Se forms for future trials. We have recently shown significant preventive benefit of methylseleninic acid (MSeA) and Se-methylselenocysteine (MSeC) in the transgenic adenocarcinoma mouse prostate (TRAMP) model by oral administration. The present work applied iTRAQ proteomic approach to profile protein changes of the TRAMP prostate and to characterize their modulation by MSeA and MSeC to identify their potential molecular targets. Dorsolateral prostates from wild-type mice at 18 weeks of age and TRAMP mice treated with water (control), MSeA, or MSeC (3 mg Se/kg) from 8 to 18 weeks of age were pooled (9-10 mice per group) and subjected to protein extraction, followed by protein denaturation, reduction, and alkylation. After tryptic digestion, the peptides were labeled with iTRAQ reagents, mixed together, and analyzed by two-dimensional liquid chromatography/tandem mass spectrometry. Of 342 proteins identified with >95% confidence, the expression of 75 proteins was significantly different between TRAMP and wild-type mice. MSeA mainly affected proteins related to prostate functional differentiation, androgen receptor signaling, protein (mis)folding, and endoplasmic reticulum-stress responses, whereas MSeC affected proteins involved in phase II detoxification or cytoprotection, and in stromal cells. Although MSeA and MSeC are presumed precursors of methylselenol and were equally effective against the TRAMP model, their distinct affected protein profiles suggest biological differences in their molecular targets outweigh similarities. Cancer Prev Res; 3(8); 994-1006. ©2010 AACR.

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“…This followed the induction of CHOP and the loss of full-length caspase-12 at 48 h, further supporting the role of these two proteins in the apoptotic effect of CLA. Previous studies have demonstrated the proapoptotic activity of CHOP (11,31,32) as well as the ability of other chemopreventive agents to induce it, including retinoids (33), phenethylisothiocyanate (34), curcumin (35), selenium (36,37), and celecoxib (38). Our study not only adds another chemopreventive agent to this list but, more importantly, extends the studies with the other agents to demonstrate that the potent induction of CHOP by CLA most likely involves the induction of XBP1, which directly regulates its transcription (11).…”

Section: The C9t11 Isomer Of Cla Does Not Disrupt Er Homeostasis or mentioning

confidence: 99%

Apoptosis induced by t10,c12-conjugated linoleic acid is mediated by an atypical endoplasmic reticulum stress response

et al. 2008

Journal of Lipid Research

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Conjugated linoleic acid (CLA) inhibits rat mammary carcinogenesis, in part by inducing apoptosis of preneoplastic and neoplastic mammary epithelial cells. The current study focused on the mechanism by which apoptosis is induced. In TM4t mammary tumor cells, trans-10,cis-12 (t10,c12)-CLA induced proapoptotic C/EBP-homologous protein (CHOP) concurrent with the cleavage of poly(ADPribose) polymerase. Knockdown of CHOP attenuated t10,c12-CLA-induced apoptosis. Furthermore, t10,c12-CLA induced the cleavage of endoplasmic reticulum (ER)-resident caspase-12, and a selective inhibitor of caspase-12 significantly alleviated t10,c12-CLA-induced apoptosis. Using electron microscopy, we observed that t10,c12-CLA treatment resulted in marked dilatation of the ER lumen. Together, these data suggest that t10,c12-CLA induces apoptosis through ER stress. To further explore the ER stress pathway, we examined the expression of the following upstream ER stress signature markers in response to CLA treatment: X-box binding protein 1 (XBP1) mRNA (unspliced and spliced), phospho-eukaryotic initiation factor (eIF) 2a, activating transcription factor 4 (ATF4), and BiP proteins. We found that t10,c12-CLA induced the expression and splicing of XBP1 mRNA as well as the phosphorylation of eIF2a. In contrast, ATF4 was induced modestly, but not significantly, and BiP was not altered. In summary, our data demonstrate that apoptosis induced by t10,c12-CLA is mediated, at least in part, through an atypical ER stress response that culminates in the induction of CHOP and the cleavage of caspase-12.-Ou, L., Y. Wu, C. Ip, X. Meng, Y-C. Hsu, and M. M. Ip. Apoptosis induced by t10,c12-conjugated linoleic acid is mediated by an atypical endoplasmic reticulum stress response. J. Lipid Res. 2008. 49: 985-994.

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Enhanced selenium effect on growth arrest by BiP/GRP78 knockdown in p53-null human prostate cancer cells

Cited by 95 publications

References 49 publications

Selenium sensitizes MCF-7 breast cancer cells to doxorubicin-induced apoptosis through modulation of phospho-Akt and its downstream substrates

Selenium sensitizes MCF-7 breast cancer cells to doxorubicin-induced apoptosis through modulation of phospho-Akt and its downstream substrates

Proteomic Profiling of Potential Molecular Targets of Methyl-Selenium Compounds in the Transgenic Adenocarcinoma of Mouse Prostate Model

Apoptosis induced by t10,c12-conjugated linoleic acid is mediated by an atypical endoplasmic reticulum stress response

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