MyEF-3, a Developmentally Controlled Brain-Derived Nuclear Protein Which Specifically Interacts with Myelin Basic Protein Proximal Regulatory Sequences

Steplewski, Andrew; Krynska, Barbara; Tretiakova, Anna P.; Haas, Susan; Khalili, Kamel; Amini, Shohreh

doi:10.1006/bbrc.1997.7821

Cited by 38 publications

(33 citation statements)

References 16 publications

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“…Paternally expressed gene 10 (PEG10) is newly identified as a paternally expressed gene at human chromosome 7q21 (Ono et al, 2001), functioning as a transcriptional factor (Steplewski et al, 1998). An elevated PEG10 expression in the majority of the human HCC cells and G2/M phase of regenerating mouse liver are indicating that this gene has growth-promoting activity (Okabe et al, 2001;Tsou et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

Androgen activates PEG10 to promote carcinogenesis in hepatic cancer cells

Xiong

Chen

et al. 2007

Oncogene

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The molecular mechanism of striking higher prevalence of hepatocellular carcinoma (HCC) in male subjects has not yet been fully elucidated. Here, we report that androgen receptor (AR) is differentially expressed in different HCC cell lines. AR agonist dihydrotestosterone (DHT) enhances HCC cell growth and apoptotic resistance. Antagonist flutamide (FLU) blocks the effects of DHT on the HCC cell lines. Paternally expressed gene 10 (PEG10) is expressed in HCC cell lines at substantial high level. Using small interfering RNAs against AR and PEG10 in AR-and PEG10-expressing BEL-7404 hepatoma cells and HuH7 hepatoma cells (HuH7) cells, and AR-transfection technique in AR-lacking and PEG10-expressing HepG2 cells, we have confirmed that through upregulation and activation of PEG10, DHT enhances HCC cell growth and apoptotic resistance. We have further demonstrated that DHT upregulates expression of human telomerase reverse transcriptase (hTERT) in HCC cell lines in a PEG10-dependent manner. Moreover, AR directly interacts in vivo with androgen-responsive elements in the regions of promoter and exon 2 of PEG10 gene in HCC cell lines. DHT promotes the hepatoma formation in vivo nude mice through PEG10 activation. AR antagonists (FLU and valproate) inhibit the hepatoma formation. These findings suggest that PEG10 plays an essential role in hepatocarcinogenesis. The PEG10 inhibition can be a novel approach for therapy of HCC.

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Section: Introductionmentioning

confidence: 99%

Androgen activates PEG10 to promote carcinogenesis in hepatic cancer cells

Xiong

Chen

et al. 2007

Oncogene

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“…PEG10 is identi ed as a maternally-imprinted and paternally expressed gene located at human chromosome 7q21 that functions as a transcriptional factor [3,7]. Our previous reports have demonstrated that B-ALL CCL19/CCR7 and CXCL13/CXCR5 together upregulate PEG10 expression, and result in the enhancement of the apoptotic resistance of B-ALL CD23+CD5+B cells [11].…”

Section: Discussionmentioning

confidence: 99%

“…Overexpression of PEG10 decreases the cell death mediated by SIAH1, a mediator of apoptosis [6]. PEG10 also appears to be important during placental development and during brain development [7][8][9].…”

mentioning

confidence: 99%

PEG10 promotes the migration of human Burkitt’s lymphoma cells by up-regulating the expression of matrix metalloproteinase-2 and -9

Xiong

Qin²,

Zheng³

et al. 2012

CIM

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* ese authors contributed equally to this work PEG10 promotes the migration of human Burkitt's lymphoma cells by up-regulating the expression of matrix metalloproteinase-2 and -9 Abstract Purpose: Paternally expressed gene 10 (PEG10) is important for apoptosis resistance in cancer cells; however, the e ect of PEG10 on tumor cell migration remains poorly understood. In this study, we investigated the e ects of PEG10 on proliferation, apoptosis, adhesion and migration in the Burkitt's lymphoma cell line, Raji.Methods: Apoptosis was induced by 5-uorouracil (5-FU) in pcDNA3.0/PEG10 transiently transfected HEK293T cells and PEG10-suppressed Raji cells. siRNAPEG10 was used to inhibit PEG10 expression. Fluorescence-activated cell sorting (FACS) were performed to analyze the e ect of PEG10 on apoptosis. CCK-8 were performed to detect cell proliferation and adhesion. Matrigel invasion were performed using PEG10-suppressed Raji cells to investigate cell migration. e expression levels of matrix metalloproteinases -2 and -9 (MMP-2 and MMP-9) were analyzed in PEG10-suppressed Raji cells using both real-time RT-PCR and Western blot analysis.Results: HEK293T cells that overexpressed PEG10 exhibited greater viability 48 h following treatment with 5-FU, relative to control cells. Speci c inhibition of PEG10 expression by siRNA resulted in inhibition of growth and apoptosis in Raji cells. Adherence and invasion capabilities were downregulated and expression levels of MMP-2 and MMP-9 were reduced in PEG10-suppressed Raji cells.Conclusions: Our ndings demonstrated that PEG10 enhances the apoptotic resistance and viability of Raji cells. e migration and adherence invasion capacity of Raji cells could potentially be a ected by regulation of the expression of MMP-2 and MMP-9. Our research provides a promising strategy for cancer immunotherapy of lymphoma.

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“…33 MyEF-3, the mouse homolog of PEG10, plays a role during brain development by interaction with myelin basic protein MB 1 domain. 34 Recently, an interaction of PEG10 with the TGF-b type I receptor ALK1 was described. 32 PEG10 overexpression has been reported in hepatocellular carcinoma and regenerating mouse liver as well as in embryonic biliary atresia.…”

Section: -Fold Compared To Normal Peripheral Blood Mononuclear Cells mentioning

confidence: 99%

“…HepG2 were stained in parallel and served as positive controls. 30,31,34 Negative controls were included in each experiment by omitting the first antibody and by using nonimmune mouse IgG. After 3 washes in PBS, preparations were evaluated by fluorescence microscopy and photographed by a digital camera using an equal exposure time.…”

Section: Peg10 Immunofluorescence Stainingmentioning

confidence: 99%

Overexpression of the paternally expressed gene 10 (PEG10) from the imprinted locus on chromosome 7q21 in high‐risk B‐cell chronic lymphocytic leukemia

Kainz

Shehata

Bilban

et al. 2007

Intl Journal of Cancer

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We report high expression of the maternally imprinted gene PEG10 in high-risk B-CLL defined by high LPL mRNA expression. Differential expression was initially identified by microarray analysis and confirmed by real time PCR in 42 B-CLL patients. mRNA expression ranged from 0.3-to 375.4-fold compared to normal peripheral blood mononuclear cells (PBMNC). Expression levels in CD19 1 B-CLL cells were 100-fold higher than in B-cells from healthy donors. PEG10 expression levels in B-CLL patient samples remained stable over time even after chemotherapy. High PEG10 expression correlated with high LPL expression (p 5 0.001) and a positive Coombs' test (p 5 0.04). Interestingly, similar expression patterns were observed for the neighbouring imprinted gene sarcoglycan-e (SGCE). Monoallelic expression and maintained imprinting of PEG10 were found by allele-or methylation-specific PCR. The intensity of intracellular staining of PEG10 protein corresponded to mRNA levels as confirmed by immunofluorescence staining. Short term knock-down of PEG10 in B-CLL cells and HepG2 cells was not associated with changes in cell survival but resulted in a significant change in the expression of 80 genes. However, long term inhibition of PEG10 led to induction of apoptosis in B-CLL cells. Our data indicate (i) a prognostic value of PEG10 in B-CLL patients; (ii) specific deregulation of the imprinted locus at 7q21 in high-risk B-CLL; (iii) a potential functional and biological role of PEG10 protein expression. Altogether, PEG10 represents a novel marker in B-CLL. ' 2007 Wiley-Liss, Inc.

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MyEF-3, a Developmentally Controlled Brain-Derived Nuclear Protein Which Specifically Interacts with Myelin Basic Protein Proximal Regulatory Sequences

Cited by 38 publications

References 16 publications

Androgen activates PEG10 to promote carcinogenesis in hepatic cancer cells

Androgen activates PEG10 to promote carcinogenesis in hepatic cancer cells

PEG10 promotes the migration of human Burkitt’s lymphoma cells by up-regulating the expression of matrix metalloproteinase-2 and -9

Overexpression of the paternally expressed gene 10 (PEG10) from the imprinted locus on chromosome 7q21 in high‐risk B‐cell chronic lymphocytic leukemia

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