ERp29 is a Radiation-Responsive Gene in IEC-6 Cell

Zhang, Bo; Wang, Meng; Yang, Yuan; Wang, Yan; Pang, Xiaowu; Su, Yongping; Wang, Junping; Ai, Guoping; Zou, Zhongmin

doi:10.1269/jrr.08014

Cited by 28 publications

(25 citation statements)

References 30 publications

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“…Patients carrying the C/C genotype have no binding sites for this factor. XBP1 is a basic leucine zipper (b-zip) TF [32,33], which is activated by cellular stress (i.e. hypoxia, DNA damage).…”

Section: Discussionmentioning

confidence: 99%

An EZH2 polymorphism is associated with clinical outcome in metastatic colorectal cancer patients

et al. 2012

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Background: Despite therapeutic innovations, metastatic colorectal cancer (mCRC) is still characterized by poor prognosis and few molecular markers predict the risk of progression. Polycomb group genes (PcGs) are epigenetic modifiers involved in tumor suppressor gene silencing. PcG member EZH2 mediates gene silencing through histone-H3 lysine-27 methylation. In colorectal cancer (CRC), EZH2 overexpression predicts shorter survival. Recently, four EZH2 single-nucleotide polymorphisms (SNPs) have been described. The present study was aimed at evaluating the correlation between EZH2 SNPs and outcome parameters in mCRC patients.Patients and methods: DNA was extracted from blood samples of 110 mCRC patients treated with first-line 5-fluorouracil, folinic acid, irinotecan (FOLFIRI) and bevacizumab. Genotyping was carried out by real-time PCR. Genotype was used to predict objective response, progression-free survival (PFS) and overall survival (OS). EZH2 messenger RNA levels were evaluated on lymphocytes of a parallel cohort of 50 CRC patients.Results: One allelic variant (rs3757441 C/C versus C/T or T/T) was significantly associated with shorter PFS and OS (P < 0.01 and P < 0.05, respectively). At multivariate analysis, the same variant resulted an independent predictor of PFS and OS (P < 0.05). The C/C variant was associated with significantly higher EZH2 expression (P < 0.05).Conclusion: An EZH2 SNP may be useful to predict clinical outcome in mCRC patients.

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Section: Discussionmentioning

confidence: 99%

An EZH2 polymorphism is associated with clinical outcome in metastatic colorectal cancer patients

et al. 2012

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“…Radiation is known to induce a series of biochemical events in the cell, but whether radiation directly induces ER stress remains unclear. Recent reports have demonstrated that radiation induces expression of ERp29, a type of ER-resident chaperone, in several types of cultured cells [7]. UPR is rapidly sensitive to environmental or physical changes.…”

Section: Introductionmentioning

confidence: 99%

Silkworm Hemolymph Down-Regulates the Expression of Endoplasmic Reticulum Chaperones under Radiation-Irradiation

Lee

Kim

et al. 2011

IJMS

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We demonstrated that up-regulation of gene expression of endoplasmic reticulum (ER) chaperones (BiP, calnexin, calreticulin, ERp29) and ER membrane kinases (IRE1, PERK, ATF6) was induced by radiation in neuronal PC12 cells. However, addition of silkworm, Bombyx mori, hemolymph to irradiated cells resulted in an obvious decrease in expression of these genes, compared with a single radiation treatment. In contrast, one of the ER chaperones, “ischemia-responsive protein 94 kDa” (irp94), was up-regulated by radiation. However, addition of silkworm hemolymph resulted in no change in the expression of irp94, with an expression pattern that differed from that of ER chaperones. Based on these results, we propose that silkworm hemolymph contains factors that regulate a decrease in the expression of ER chaperones under radiation-irradiation conditions, with the exception of irp94, which is not down-regulated. We suggest that this difference in the molecular character of irp94 may provide a clue to the biological functions associated with ER stress pathways, particularly the effects of radiation.

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“…18 It has been shown that ERp29 is directly associated with the folding and/or secretion of thyroglobulin, 19 as well as resistance to oxidative and radiation stress. 20,21 Importantly, it was found to be highly expressed in primary tumor and cell lines. [22][23][24] Recent findings that ERp29 expression correlated with tumor growth rate 24 and knockdown of ERp29 by siRNA in noninvasive MCF-7 breast cancer cells attenuated tumorigenesis 25 imply an oncogenic role of ERp29 in breast tumor formation.…”

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confidence: 99%

Overexpression of endoplasmic reticulum protein 29 regulates mesenchymal–epithelial transition and suppresses xenograft tumor growth of invasive breast cancer cells

Bambang

Zhou

et al. 2009

Laboratory Investigation

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Endoplasmic reticulum protein 29 (ERp29) is a novel endoplasmic reticulum (ER) secretion factor that facilitates the transport of secretory proteins in the early secretory pathway. Recently, it was found to be overexpressed in several cancers; however, little is known regarding its function in breast cancer progression. In this study, we show that the expression of ERp29 was reduced with tumor progression in clinical specimens of breast cancer, and that overexpression of ERp29 resulted in G 0 /G 1 arrest and inhibited cell proliferation in MDA-MB-231 cells. Importantly, overexpression of ERp29 in MDA-MB-231 cells led to a phenotypic change and mesenchymal-epithelial transition (MET) characterized by cytoskeletal reorganization with loss of stress fibers, reduction of fibronectin (FN), reactivation of epithelial cell marker E-cadherin and loss of mesenchymal cell marker vimentin. Knockdown of ERp29 by shRNA in MCF-7 cells reduced E-cadherin, but increased vimentin expression. Furthermore, ERp29 overexpression in MDA-MB-231 and SKBr3 cells decreased cell migration/invasion and reduced cell transformation, whereas silencing of ERp29 in MCF-7 cells enhanced cell aggressive behavior. Significantly, expression of ERp29 in MDA-MB-231 cells suppressed tumor formation in nude mice by repressing the cell proliferative index (Ki-67 positivity). Transcriptional profiling analysis showed that ERp29 acts as a central regulator by upregulating a group of genes with tumor suppressive function, for example, E-cadherin (CDH1), cyclin-dependent kinase inhibitor (CDKN2B) and spleen tyrosine kinase (SYK), and by downregulating a group of genes that regulate cell proliferation (eg, FN, epidermal growth factor receptor (EGFR) and plasminogen activator receptor (uPAR)). It is noteworthy that ERp29 significantly attenuated the overall ERK cascade, whereas the ratio of p-ERK1 to p-ERK2 was highly increased. Taken together, our results showed that ERp29 is a novel regulator leading to cell growth arrest and cell transition from a proliferative to a quiescent state, and reprogramming molecular portraits to suppress the tumor growth of MDA-MB-231 breast cancer cells.

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ERp29 is a Radiation-Responsive Gene in IEC-6 Cell

Cited by 28 publications

References 30 publications

An EZH2 polymorphism is associated with clinical outcome in metastatic colorectal cancer patients

An EZH2 polymorphism is associated with clinical outcome in metastatic colorectal cancer patients

Silkworm Hemolymph Down-Regulates the Expression of Endoplasmic Reticulum Chaperones under Radiation-Irradiation

Overexpression of endoplasmic reticulum protein 29 regulates mesenchymal–epithelial transition and suppresses xenograft tumor growth of invasive breast cancer cells

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