Epigenetic status of H19/IGF2 and SNRPN imprinted genes in aborted and successfully derived embryonic stem cell lines in non-human primates

Wianny, Florence; Blachère, Thierry; Godet, Murielle; Guillermas, Rémi; Cortay, Véronique; Bourillot, Pierre‐Yves; Lefèvre, Annick; Savatier, Pierre; Dehay, Colette

doi:10.1016/j.scr.2016.03.002

Cited by 5 publications

(2 citation statements)

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“…As one of the essential components of spliceosome, SNRP protein was differently expressed in cancer cells to exert important activities (Krausova and Stanek, 2018). Overexpression of SNRPN was identified in acute myeloid leukemia and breast cancer (Benetatos et al, 2010; Barrow et al, 2015), and functioned in the maintenance of stemness of stem cells (Wianny et al, 2016). SNRPE is overexpressed in high‐grade prostate cancer (Anchi et al, 2012).…”

Section: Discussionmentioning

confidence: 99%

c‐Myc‐mediated SNRPB upregulation functions as an oncogene in hepatocellular carcinoma

Peng

et al. 2020

Cell Biology International

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Dysregulation of genes involved in alternative splicing contributes to hepatocarcinogenesis. SNRPB, a component of spliceosome, is implicated in human cancers, yet its clinical significance and biological function in hepatocellular carcinoma (HCC) remains unknown. Here, we show that SNRPB expression is increased in HCC tissues, compared with the nontumorous tissues, at both messenger RNA and protein levels in two independent cohorts. High expression of SNRPB is significantly associated with higher pathological grade, vascular invasion, serum alpha-fetoprotein level, tumor metastasis, and poor disease-free and overall survivals. Luciferase reporter and chromatin immunoprecipitation assays demonstrate that SNRPB upregulation in HCC is mediated by c-Myc. Positive correlation is found between SNRPB and c-Myc expression in clinical samples. In vitro studies show that ectopic expression of SNRPB promotes HCC cell proliferation and migration, whereas knockdown of SNRPB results in the opposite phenotypes. Collectively, our data suggest SNRPB function as an oncogene and serve as a potential prognostic factor in HCC.

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Section: Discussionmentioning

confidence: 99%

c‐Myc‐mediated SNRPB upregulation functions as an oncogene in hepatocellular carcinoma

Peng

et al. 2020

Cell Biology International

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“…H19 is an imprinted gene that has been extensively studied and plays an important role in the formation, implantation and growth of gametes and embryos. Abnormal imprinting of H19 is one of the causes of human Beckwith-Wiedemann Syndrome (BWS) and Silver-Russell Syndrome (SRS) ( 4 , 5 ). Methylation is one of the important mechanisms in gene imprinting process.…”

Section: Introductionmentioning

confidence: 99%

Effect of abnormal GpG methylation in the second trimester of pregnancy on adverse health risk of offspring

et al. 2018

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Effect of abnormal GpG methylation in amniotic fluid cells during the second trimester of pregnancy on adverse health risk of offspring was investigated. In total, 237 sets of amniotic fluid cells were collected from patients who received prenatal diagnosis in the Third Affiliated Hospital of Guangzhou Medical University (Guangzhou, China) from April 2010 to October 2011. Among them, 156 sets were from singleton and 81 sets were from twins. H19 gene was amplified by PCR, and the product was purified and pyrosequencing was used to detect the DNA methylation level of GapG. Follow-up records of the birth outcomes of pregnant women's offspring were collected. Positive rate of DNA amplification in 200 cases of amniotic fluid cells was 84.4% (200/237). Average age of singleton pregnancies was higher than that of twins (P<0.05), and no significant differences were found in gestational age and PCR amplification rate (P>0.05). There was no difference in the methylation level of GapG between singleton and twins (P>0.05), but the abnormal methylation rate of GapG1 in twin fetuses was significantly higher than that of singleton (20.3 vs. 3.6%, χ2=8.364, P=0.004). Offspring sex, singleton or twins, mode of delivery, time of pregnancy, and low birth weight showed no significant effect on GapG methylation level of H19 in the second trimester of pregnancy. No offspring deformities were found regardless of the increased or decreased degree of methylation (P>0.05). The number of fetuses born may cause abnormal GapG1 methylation, but no effect of GapG methylation on the adverse health risk of offspring was found.

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Analysis of developmental imprinting dynamics in primates using SNP-free methods to identify imprinting defects in cloned placenta

et al. 2021

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Epigenetic status of H19/IGF2 and SNRPN imprinted genes in aborted and successfully derived embryonic stem cell lines in non-human primates

Cited by 5 publications

References 71 publications

c‐Myc‐mediated SNRPB upregulation functions as an oncogene in hepatocellular carcinoma

c‐Myc‐mediated SNRPB upregulation functions as an oncogene in hepatocellular carcinoma

Effect of abnormal GpG methylation in the second trimester of pregnancy on adverse health risk of offspring

Analysis of developmental imprinting dynamics in primates using SNP-free methods to identify imprinting defects in cloned placenta

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