DNA methyltransferases and tRNA methyltransferase DNMT2 in developing pig brain - expression and promoter methylation

Gene Reports ◽  
2018 ◽  
Vol 11 ◽  
pp. 42-51
Author(s):  
Knud Larsen ◽  
Kaja Kjær Kristensen ◽  
Henrik Callesen
Keyword(s):  
Promoter Methylation ◽  
Dna Methyltransferases ◽  
Pig Brain ◽  
Brain Expression ◽  
Trna Methyltransferase

scholarly journals Lack of TNFα expression protects anaplastic lymphoma kinase-positive T-cell lymphoma (ALK+ TCL) cells from apoptosis

2009 ◽  
Vol 106 (37) ◽  
pp. 15843-15848 ◽  
Author(s):  
Qian Zhang ◽  
Hong Y. Wang ◽  
Gauri Bhutani ◽  
Xiaobin Liu ◽  
Michele Paessler ◽  
...  
Keyword(s):  
Dna Methylation ◽  
T Cell ◽  
Cell Lines ◽  
Promoter Methylation ◽  
Anaplastic Lymphoma Kinase ◽  
Dna Methyltransferase ◽  
Dna Methyltransferases ◽  
Luciferase Reporter ◽  
Dependent Manner ◽  
Anaplastic Lymphoma

Here we report that T-cell lymphomas characterized by the expression of anaplastic lymphoma kinase (ALK+ TCL) fail to express the TNFα and frequently display DNA methylation of the TNFα gene promoter. While only a subset of the ALK+ TCL-derived cell lines showed a high degree of the promoter methylation, all 6 showed low to nondetectable expression of the TNFα mRNA, and none expressed the TNFα protein. All 14 ALK+ TCL tissue samples examined displayed some degree of the TNFα promoter methylation, which was the most prominent in the distal portion of the the promoter. Treatment with a DNA methyltransferase inhibitor, 5′-aza-2′-deoxy-cytidine (5-ADC), reversed the promoter methylation and led to the expression of TNFα mRNA and protein. Furthermore, in vitro DNA methylation of the promoter impaired its transcriptional activity in the luciferase reporter assay. This impairment was seen even if only either distal or proximal portion were methylated, with methylation of the former exerting a more profound inhibitory effect. Notably, the ALK+ TCL cell lines uniformly expressed the type 1 TNFα receptor (TNF-R1) protein known to transduce the TNFα-induced pro-apoptotic signals. Moreover, exogeneous TNFα inhibited growth of the ALK+ TCL cell lines in a dose-dependent manner and induced activation of the members of the cell apoptotic pathway: Caspase 8 and caspase 3. These findings provide additional rationale for the therapeutic inhibition of DNA methyltransferases in ALK+ TCL. They also suggest that treatment with TNFα may be highly effective in this type of lymphoma.

Altered DNA methyltransferases promoter methylation and mRNA expression are associated with tamoxifen response in breast tumors

2018 ◽  
Vol 233 (9) ◽  
pp. 7305-7319 ◽  
Author(s):  
Rosa Jahangiri ◽  
Fatemeh Mosaffa ◽  
Amirnader Emami Razavi ◽  
Ladan Teimoori-Toolabi ◽  
Khadijeh Jamialahmadi
Keyword(s):  
Mrna Expression ◽  
Promoter Methylation ◽  
Breast Tumors ◽  
Dna Methyltransferases ◽  
Tamoxifen Response

Delineation of Promoter Methylation in Patients with Myelodysplastic Syndromes: Widespread and Concurrent Hypermethylation of Multiple Genes and Increased mRNA Expression of the DNA Methyltransferases DNMT1, 3A and 3B.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 472-472
Author(s):  
Anni Aggerholm ◽  
Mette S. Holm ◽  
Per Guldberg ◽  
Peter Hokland
Keyword(s):  
Bone Marrow ◽  
Disease Progression ◽  
Myelodysplastic Syndromes ◽  
Promoter Methylation ◽  
Methylation Status ◽  
Promoter Hypermethylation ◽  
Dna Methyltransferases ◽  
Aberrant Methylation ◽  
Mrna Levels ◽  
Over Time

Abstract Transcriptional silencing of tumor suppressor genes by promoter hypermethylation is associated with hematological malignancy, including myelodysplastic syndromes (MDS). Specifically, hypermethylation of the p15 gene has previously been associated with MDS and seems to be acquired with disease progression. The methylation status of other genes associated with the development of myeloid malignancies is, however, largely unknown. We have elucidated this in total bone marrow mononuclear cells (BM-MNC) as well as CD34 enriched cells from 17 patients with different stages of MDS by determining the promoter methylation status in four genes believed to be associated with the development of acute myeloid leukemia (AML), namely those encoding for the p15, HIC, E-cadherin (ECAD), and the Estrogen receptor (ER). Employing Bisulfite-Denaturing Gradient Gel Electrophoresis (Bisulfite-DGGE) we found all four genes to be hypermethylated in MDS, albeit with varying frequencies (19/37, 12/37, 10/37, and 7/37, respectively). Since the Bisulfite-DGGE allows for the detection of heterogeneous methylation patterns we were able to compare these patterns. Similar Bisulfite-DGGE band patterns were observed in total BM-MNC and CD34 cells in all positive patients suggesting that methylation is a process encompassing both immature and end-stage hematopoietic cells. In a total of 37 patients (14 RA, 3 RAS, 11 RAEB, 4 RAEB-t and 5 with AML secondary to MDS) analyzed, we found promoter hypermethylation of the HIC gene to be significantly increased in advanced MDS (p<0.05). To determine the kinetics of promoter methylation in the single patient, bone marrow from eleven MDS patients, where two or more samples were available, were analyzed (observation time between sampling ranged from 43 to 1132 days, median 284 days). These analyses showed that the patterns of methylation are surprisingly stable over time. When two or more samples were analyzed we found that the number of methylated genes only changed in three of the eleven patients. To delineate the process of hypermethylation we determined the mRNA levels of the DNA methyltransferases (DNMT) 1, 3A, and 3B. Interestingly, all three DNMTs were up-regulated in MDS compared to normal bone marrow (DNMT1 and DNMT3A: p<0.01; DNMT3B: p<0.0001) and DNMT3A and 3B were up-regulated in advanced MDS compared to low-risk MDS (p<0.01). Taken together, these results imply an involvement of promoter hypermethylation in MDS disease progression, and DNMT overexpression as a contributing factor for the aberrant methylation in these patients. Figure: Promoter hypermethylation status over time. A) Development in methylation status in 11 patients. Arrows indicate patients where methylation status changes over time. a) RA, b) RAS, c) RAEB, d) RAEB-t, e) sAML. Black quarters: methylated; white quarters: unmethylated. B) Bisulfite-DGGE experiments for methylation in the p15, HIC , and ER promoters in UPN 2. Figure Figure

Abstract #60: PTEN Promoter Methylation is Specifically Detected in Differentiated Thyroid Cancers

2003 ◽  
Vol 9 ◽  
pp. 23-24
Author(s):  
Francisco Alvarez ◽  
Helena Bussaglia ◽  
Monica Vilar ◽  
Juan Ybarra ◽  
Alberto de Leiva ◽  
...  
Keyword(s):  
Promoter Methylation ◽  
Thyroid Cancers ◽  
Differentiated Thyroid Cancers

GPER is inactivated by promoter methylation and potentially functions as a tumor suppressor in breast cancer

2014 ◽  
Vol 74 (S 01) ◽  
Author(s):  
C Weißenborn ◽  
T Ignatov ◽  
SD Costa ◽  
AC Zenclussen ◽  
A Ignatov
Keyword(s):  
Breast Cancer ◽  
Tumor Suppressor ◽  
Promoter Methylation

Opiate-binding in the developing pig brain

1988 ◽  
Vol 117 (4_Suppl) ◽  
pp. S112-S113
Author(s):  
N. PARVIZI
Keyword(s):  
Pig Brain ◽  
Opiate Binding
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