scholarly journals MicroRNA-148a can regulate runt-related transcription factor 3 gene expression via modulation of DNA methyltransferase 1 in gastric cancer

2013 ◽  
Vol 35 (4) ◽  
pp. 313-319 ◽  
Author(s):  
Junbo Zuo ◽  
Jiazeng Xia ◽  
Feng Ju ◽  
Jiang Yan ◽  
Akao Zhu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Gastric Cancer ◽  
Transcription Factor ◽  
Dna Methyltransferase ◽  
Dna Methyltransferase 1 ◽  
Related Transcription Factor ◽  
Methyltransferase 1 ◽  
Transcription Factor 3

scholarly journals Alteration in the expression of MGMT and RUNX3 due to non-CpG promoter methylation and their correlation with different risk factors in esophageal cancer patients

Tumor Biology ◽  
2017 ◽  
Vol 39 (5) ◽  
pp. 101042831770163 ◽  
Author(s):  
Snigdha Saikia ◽  
Asad Ur Rehman ◽  
Prajjalendra Barooah ◽  
Preeti Sarmah ◽  
Mallika Bhattacharyya ◽  
...  
Keyword(s):  
Esophageal Cancer ◽  
Transcription Factor ◽  
Promoter Methylation ◽  
Messenger Rna ◽  
Dna Methyltransferase ◽  
Rna Expression ◽  
Betel Nut ◽  
Methylguanine Dna Methyltransferase ◽  
Related Transcription Factor ◽  
Transcription Factor 3

Promoter methylation reflects in the inactivation of different genes like O6-methylguanine-DNA methyltransferase DNA repair gene and runt-related transcription factor 3, a known tumor suppressor gene in various cancers such as esophageal cancer. The promoter methylation was evaluated for O6-methylguanine-DNA methyltransferase and runt-related transcription factor 3 in CpG, CHH, and CHG context (where H is A, T, or C) by next-generation sequencing. The methylation status was correlated with quantitative messenger RNA expression. In addition, messenger RNA expression was correlated with different risk factors like tobacco, alcohol, betel nut consumption, and smoking habit. CpG methylation of O6-methylguanine-DNA methyltransferase promoter had a positive association in the development of esophageal cancer (p < 0.05), whereas runt-related transcription factor 3 promoter methylation showed no significant association (p = 1.0) to develop esophageal cancer. However, the non-CpG methylation, CHH, and CHG were significantly correlated with O6-methylguanine-DNA methyltransferase (p < 0.05) and runt-related transcription factor 3 (p < 0.05) promoters in the development of esophageal cancer. The number of cytosine converted to thymine (C→T) in O6-methylguanine-DNA methyltransferase promoter showed a significant correlation between cases and controls (p < 0.05), but in runt-related transcription factor 3 no such significant correlation was observed. Besides, messenger RNA expression was found to be significantly correlated with promoter hypermethylation of O6-methylguanine-DNA methyltransferase and runt-related transcription factor 3 in the context of CHG and CHH (p < 0.05). The CpG hypermethylation in O6-methylguanine-DNA methyltransferase showed positive (p < 0.05) association, whereas in runt-related transcription factor 3, it showed contrasting negative association (p = 0.23) with their messenger RNA expression. Tobacco, betel nut consumption, and smoking habits were associated with altered messenger RNA expression of O6-methylguanine-DNA methyltransferase (p < 0.05) and betel nut consumption and smoking habits were associated with runt-related transcription factor 3 (p < 0.05). There was no significant association between messenger RNA expression of O6-methylguanine-DNA methyltransferase and runt-related transcription factor 3 with alcohol consumption (p = 0.32 and p = 0.15). In conclusion, our results suggest that an aberrant messenger RNA expression may be the outcome of CpG, CHG, and CHH methylation in O6-methylguanine-DNA methyltransferase, whereas outcome of CHG and CHH methylation in runt-related transcription factor 3 promoters along with risk factors such as consumption of tobacco, betel nut, and smoking habits in esophageal cancer from Northeast India.

MicroRNA-148a is silenced by hypermethylation and interacts with DNA methyltransferase 1 in gastric cancer

2011 ◽  
Vol 29 (4) ◽  
pp. 2701-2709 ◽  
Author(s):  
Akao Zhu ◽  
Jiazeng Xia ◽  
Junbo Zuo ◽  
Shimao Jin ◽  
Hong Zhou ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Dna Methyltransferase ◽  
Dna Methyltransferase 1 ◽  
Methyltransferase 1

scholarly journals EGCG Prevents High Fat Diet-Induced Changes in Gut Microbiota, Decreases of DNA Strand Breaks, and Changes in Expression and DNA Methylation ofDnmt1andMLH1in C57BL/6J Male Mice

2017 ◽  
Vol 2017 ◽  
pp. 1-17 ◽  
Author(s):  
Marlene Remely ◽  
Franziska Ferk ◽  
Sonja Sterneder ◽  
Tahereh Setayesh ◽  
Sylvia Roth ◽  
...  
Keyword(s):  
Gene Expression ◽  
Dna Methylation ◽  
Dna Damage ◽  
Gut Microbiota ◽  
High Fat Diet ◽  
Dna Methyltransferase ◽  
Dna Methyltransferase 1 ◽  
Male Mice ◽  
High Fat ◽  
Methyltransferase 1

Obesity as a multifactorial disorder involves low-grade inflammation, increased reactive oxygen species incidence, gut microbiota aberrations, and epigenetic consequences. Thus, prevention and therapies with epigenetic active antioxidants, (-)-Epigallocatechin-3-gallate (EGCG), are of increasing interest. DNA damage, DNA methylation and gene expression ofDNA methyltransferase 1,interleukin 6, andMutL homologue 1were analyzed in C57BL/6J male mice fed a high-fat diet (HFD) or a control diet (CD) with and without EGCG supplementation. Gut microbiota was analyzed with quantitative real-time polymerase chain reaction. An induction of DNA damage was observed, as a consequence of HFD-feeding, whereas EGCG supplementation decreased DNA damage. HFD-feeding induced a higher inflammatory status. Supplementation reversed these effects, resulting in tissue specific gene expression and methylation patterns ofDNA methyltransferase 1andMutL homologue 1. HFD feeding caused a significant lower bacterial abundance. TheFirmicutes/Bacteroidetesratio is significantly lower in HFD + EGCG but higher in CD + EGCG compared to control groups. The results demonstrate the impact of EGCG on the one hand on gut microbiota which together with dietary components affects host health. On the other hand effects may derive from antioxidative activities as well as epigenetic modifications observed on CpG methylation but also likely to include other epigenetic elements.

scholarly journals Chromium Cross-Links Histone Deacetylase 1-DNA Methyltransferase 1 Complexes to Chromatin, Inhibiting Histone-Remodeling Marks Critical for Transcriptional Activation

2007 ◽  
Vol 27 (20) ◽  
pp. 7089-7101 ◽  
Author(s):  
Michael Schnekenburger ◽  
Glenn Talaska ◽  
Alvaro Puga
Keyword(s):  
Gene Expression ◽  
Histone Deacetylase ◽  
Dna Methyltransferase ◽  
Epigenetic Modification ◽  
Dna Methyltransferase 1 ◽  
Transcriptional Responses ◽  
Histone Deacetylase 1 ◽  
Environmental Agents ◽  
Cross Links ◽  
Methyltransferase 1

ABSTRACT Transcriptional regulation of gene expression requires posttranslational modification of histone proteins, which, in concert with chromatin-remodeling factors, modulate chromatin structure. Exposure to environmental agents may interfere with specific histone modifications and derail normal patterns of gene expression. To test this hypothesis, we coexposed cells to binary mixtures of benzo[a]pyrene (B[a]P), an environmental procarcinogen that activates Cyp1a1 transcriptional responses mediated by the aryl hydrocarbon receptor (AHR), and chromium, a carcinogenic heavy metal that represses B[a]P-inducible AHR-mediated gene expression. We show that chromium cross-links histone deacetylase 1-DNA methyltransferase 1 (HDAC1-DNMT1) complexes to Cyp1a1 promoter chromatin and inhibits histone marks induced by AHR-mediated gene transactivation, including phosphorylation of histone H3 Ser-10, trimethylation of H3 Lys-4, and various acetylation marks in histones H3 and H4. These changes inhibit RNA polymerase II recruitment without affecting the kinetics of AHR DNA binding. HDAC1 and DNMT1 inhibitors or depletion of HDAC1 or DNMT1 with siRNAs blocks chromium-induced transcriptional repression by decreasing the interaction of these proteins with the Cyp1a1 promoter and allowing histone acetylation to proceed. By inhibiting Cyp1a1 expression, chromium stimulates the formation of B[a]P DNA adducts. Epigenetic modification of gene expression patterns may be a key element of the developmental and carcinogenic outcomes of exposure to chromium and to other environmental agents.

scholarly journals Gene Expression Pattern and Downregulation of DNA Methyltransferase 1 Using siRNA in Porcine Somatic Cells

2009 ◽  
Vol 14 (5) ◽  
pp. 251-263 ◽  
Author(s):  
ANGELICA M. GIRALDO ◽  
TODD D. VAUGHT ◽  
LIMIN FU ◽  
ALISON J. DUNCAN ◽  
AMY M. VANCE ◽  
...  
Keyword(s):  
Gene Expression ◽  
Expression Pattern ◽  
Dna Methyltransferase ◽  
Somatic Cells ◽  
Gene Expression Pattern ◽  
Dna Methyltransferase 1 ◽  
Methyltransferase 1

scholarly journals Polymorphisms of the DNA Methyltransferase 1 Gene Predict Survival of Gastric Cancer Patients Receiving Tumorectomy

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Zhifang Jia ◽  
Xing Wu ◽  
Donghui Cao ◽  
Chuan Wang ◽  
Lili You ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Overall Survival ◽  
Dna Methyltransferase ◽  
Cox Regression ◽  
Methylation Status ◽  
Dna Methyltransferase 1 ◽  
Cox Regression Analysis ◽  
Independent Prognostic Marker ◽  
Gastric Cancer Patients ◽  
Methyltransferase 1

DNA methyltransferase 1 (DNMT1) plays a pivotal role in maintaining DNA methylation status. Polymorphisms ofDNMT1may modify the role of DNMT1 in prognosis of gastric cancer (GC). Our aim was to test whether polymorphisms ofDNMT1gene were associated with overall survival of GC. Four hundred and forty-seven GC patients who underwent radical tumorectomy were enrolled in the study. Five tagging SNPs (rs10420321, rs16999593, rs2228612, rs2228611, and rs2288349) of theDNMT1gene were genotyped by TaqMan assays. Kaplan-Meier survival plots and Cox proportional hazard regression were used to analyze the associations between SNPs ofDNMT1and survival of GC. Patients carrying rs2228611 GA/AA genotype tended to live longer than those bearing the GG genotype (HR 0.68, 95% CI: 0.51–0.91,P=0.007). Further multivariate Cox regression analysis showed that rs2228611 was an independent prognostic factor (GA/AA versus GG: OR 0.67, 95% CI 0.49–0.91,P=0.010). Nevertheless, other SNPs did not show any significant associations with survival of GC. Polymorphisms of theDNMT1gene may affect overall survival of GC. The SNP rs2228611 has the potentiality to serve as an independent prognostic marker for GC patients.

scholarly journals Effect of 5'-fluoro-2'-deoxycytidine, 5-azacytidine, and 5-aza-2'–deoxycytidine on DNA Methyltransferase 1, CIP/KIP Family, and INK4a/ARF in Colon Cancer HCT-116 Cell Line

2022 ◽  
Vol 14 (12) ◽  
Author(s):  
Masumeh Sanaei ◽  
Fraidoon Kavoosi
Keyword(s):  
Gene Expression ◽  
Cell Cycle ◽  
Colon Cancer ◽  
Cell Growth ◽  
Cell Line ◽  
Dna Methyltransferase ◽  
Negative Regulator ◽  
Dna Methyltransferase 1 ◽  
Hct 116 ◽  
Methyltransferase 1

Background: Cyclin-dependent kinase inhibitors (CKIs) are the negative regulator of cell cycle progression, which inhibits cyclin-cdk complexes, resulting in cell cycle arrest. Recently, we evaluated the effect of 5-Aza-CdR on DNMT1 gene expression in the WCH-17 hepatocellular carcinoma (HCC) cell line. Objectives: The current study was designed to analyze the effects of 5-aza-2'–deoxycytidine (5-Aza-CdR, decitabine), 5-azacytidine (5-AzaC, vidaza), and 5'-fluoro-2'-deoxycytidine (FdCyd) on INK4a/ARF, CIP/KIP, and DNA methyltransferase 1 gene expression, apoptosis induction, and cell growth inhibition in colon cancer HCT-116 cell line. Methods: The colon cancer HCT-116 cell line was treated with 5-azaC, 5-Aza-CdR, and FdCyd at 24 and 48h. To determine colon cancer HCT-116 cell viability, cell apoptosis, and the relative expression level of the INK4a/ARF, CIP/KIP, and DNA methyltransferase 1 genes, MTT assay, flow cytometry, and qRT-PCR were done, respectively. Results: 5-azaC, 5-Aza-CdR, and FdCyd significantly inhibited colon cancer HCT-116 cell growth and induced apoptosis. Besides, they significantly increased CIP/KIP (p21CIP1, p27KIP1, and p57KIP2) and INK4 (p14ARF, p15INK4b, and p16INK4a) and decreased DNMT1 gene expression. Besides, minimal and maximal apoptosis were seen in the groups treated with FdCyd and 5-Aza-CdR, respectively. The IC50 for CAF for FdCyd was 1.72 ± 0.23 and 1.63 ± 0.21μM at 24 and 48h, respectively. The IC50 for CAF for 5-AzaC was 2.18 ± 0.33 and 1.98 ± 0.29 μM at 24 and 48h, respectively. The IC50 for CAF for 5-Aza-CdR was 4.08 ± 0.61 and 3.18 ± 0.50 μM at 24 and 48h, respectively. Conclusions: The 5-azac, 5-Aza-CdR, and FdCyd can reactivate the INK4a/ARF and CIP/KIP families through inhibition of DNMT1 activity.

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