scholarly journals Non-Coding RNA Transcription and RNA-Directed DNA Methylation in Arabidopsis

2014 ◽  
Vol 7 (9) ◽  
pp. 1406-1414 ◽  
Author(s):  
Xin-Jian He ◽  
Ze-Yang Ma ◽  
Zhang-Wei Liu
Keyword(s):  
Dna Methylation ◽  
Rna Transcription ◽  
Non Coding Rna

ADAMTS9-AS2: A functional long non-coding RNA in tumorigenesis

2021 ◽  
Vol 27 ◽  
Author(s):  
Wen Xu ◽  
Bei Wang ◽  
Yuxuan Cai ◽  
Jinlan Chen ◽  
Xing Lv ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Signaling Pathways ◽  
Therapeutic Target ◽  
Molecular Mechanisms ◽  
Human Cancer ◽  
Migration Inhibition ◽  
Cancer Proliferation ◽  
Non Coding Rna ◽  
Non Coding Rnas ◽  
Long Non Coding Rna

Background: Long non-coding RNAs (lncRNA) have been identified as novel molecular regulators in cancers. LncRNA ADAMTS9-AS2 can mediate the occurrence and development of cancer through various ways such as regulating miRNAs, activating the classical signaling pathways in cancer, and so on, which have been studied by many scholars. In this review, we summarize the molecular mechanisms of ADAMTS9-AS2 in different human cancers. Methods: Through a systematic search of PubMed, lncRNA ADAMTS9-AS2 mediated molecular mechanisms in cancer are summarized inductively. Results: ADAMTS9-AS2 aberrantly expression in different cancers is closely related to cancer proliferation, invasion, migration, inhibition of apoptosis. The involvement of ADAMTS9-AS2 in DNA methylation, mediating PI3K / Akt / mTOR signaling pathways, regulating miRNAs and proteins, and such shows its significant potential as a therapeutic cancer target. Conclusion: LncRNA ADAMTS9-AS2 can become a promising biomolecular marker and a therapeutic target for human cancer.

scholarly journals The APT complex is involved in non-coding RNA transcription and is distinct from CPF

2018 ◽  
Author(s):  
Michael Lidschreiber ◽  
Ashley D Easter ◽  
Sofia Battaglia ◽  
Juan B Rodríguez-Molina ◽  
Ana Casañal ◽  
...  
Keyword(s):  
Rna Transcription ◽  
Non Coding Rna

scholarly journals Genetic and epigenetic associations of ANRIL with coronary artery disease and risk factors

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Bayi Xu ◽  
Zhixia Xu ◽  
Yequn Chen ◽  
Nan Lu ◽  
Zhouwu Shu ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Coronary Artery Disease ◽  
Dna Methylation ◽  
Coronary Artery ◽  
Gene Dosage ◽  
Density Lipoprotein ◽  
Nucleotide Polymorphisms ◽  
Coronary Syndrome ◽  
Non Coding Rna ◽  
Artery Disease

Abstract Background Both DNA genotype and methylation of antisense non-coding RNA in the INK4 locus (ANRIL) have been robustly associated with coronary artery disease (CAD), but the interdependent mechanisms of genotype and methylation remain unclear. Methods Eighteen tag single nucleotide polymorphisms (SNPs) of ANRIL were genotyped in a matched case–control study (cases 503 and controls 503). DNA methylation of ANRIL and the INK4/ARF locus (p14ARF, p15INK4b and p16INK4a) was measured using pyrosequencing in the same set of samples (cases 100 and controls 100). Results Polymorphisms of ANRIL (rs1004638, rs1333048 and rs1333050) were significantly associated with CAD (p < 0.05). The incidence of CAD, multi-vessel disease, and modified Gensini scores demonstrated a strong, direct association with ANRIL gene dosage (p < 0.05). There was no significant association between ANRIL polymorphisms and myocardial infarction/acute coronary syndrome (MI/ACS) (p > 0.05). Methylation levels of ANRIL were similar between the two studied groups (p > 0.05), but were different in the rs1004638 genotype, with AA and AT genotype having a higher level of ANRIL methylation (pos4, p = 0.006; pos8, p = 0.019). Further Spearman analyses indicated that methylation levels of ANRIL were positively associated with systolic blood pressure (pos6, r = 0.248, p = 0.013), diastolic blood pressure (pos3, r = 0.213, p = 0.034; pos6, r = 0.220, p = 0.028), and triglyceride (pos4, r = 0.253, p = 0.013), and negatively associated with high-density lipoprotein cholesterol (pos2, r = − 0.243, p = 0.017). Additionally, we identified 12 transcription factor binding sites (TFBS) within the methylated ANRIL region, and functional annotation indicated these TFBS were associated with basal transcription. Methylation at the INK4/ARF locus was not associated with ANRIL genotype. Conclusions These results indicate that ANRIL genotype (tag SNPs rs1004638, rs1333048 and rs1333050) mainly affects coronary atherosclerosis, but not MI/ACS. There may be allele-related DNA methylation and allele-related binding of transcription factors within the ANRIL promoter.

The interaction between DNA methylation and long non‐coding RNA during the onset of puberty in goats

2018 ◽  
Vol 53 (6) ◽  
pp. 1287-1297
Author(s):  
Chen Yang ◽  
Xiaoxiao Gao ◽  
Jing Ye ◽  
Jianping Ding ◽  
Ya Liu ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Non Coding Rna ◽  
Long Non Coding Rna

Non-coding RNA transcription: turning on neighbours

2008 ◽  
Vol 10 (9) ◽  
pp. 1023-1024 ◽  
Author(s):  
Piero Carninci
Keyword(s):  
Rna Transcription ◽  
Non Coding Rna

Epimutation of the Tumor Suppressor Mechanism in 13q14.3 Involves Monoallelic Expression, Non-Coding RNA Genes and Deregulation of NFkB Signalling

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 783-783
Author(s):  
Daniel Mertens ◽  
Angela Philippen ◽  
Nupur Bhattacharya ◽  
Cordula Tschuch ◽  
Melanie Ruppel ◽  
...  
Keyword(s):  
Dna Methylation ◽  
B Cells ◽  
Tumor Suppressor ◽  
Candidate Genes ◽  
Target Genes ◽  
Gene Copy ◽  
Loss Of Function ◽  
Non Coding Rna ◽  
Suppressor Mechanism ◽  
Rna Genes

Abstract Deletions in chromosomal band 13q14.3 occur in a variety of human neoplasms like chronic lymphocytic leukaemia (CLL), indicating a tumor suppressor mechanism (TSM) in this region. Intriguingly, several characteristics of the region of interest point to an epigenetic pathomechanism: candidate protein-coding genes and non-coding RNA genes including miR15a and miR16-1 lack point mutations in the majority of patients, yet these genes are significantly downregulated in almost all CLL patients the presence of large non-coding RNA genes in 13q14.3 is reminiscent of imprinted regions where only one gene copy is active. We have recently shown that already in healthy tissue only one gene copy of 13q14.3 is active while one gene copy is randomly chosen for silencing. Thus, loss of the single active copy is sufficient for complete loss of gene function in tumor cells. In order to elucidate the epigenetic regulatory mechanism, we analysed DNA- and Histone-methylation of all CpG islands in the region in non-malignant B-cells and CLL cells. Using aPRIMES and ChIP-qPCR as screening tools, BioCOBRA as a quantitative high-throughput method and bisulfite sequencing for validation, we could identify two candidate regulatory elements with abnormal chromatin in CLL patients (n=80, median 57% DNA-methylation, range 0–100%) as compared to healthy probands (n=20, median 88% DNA-methylation, range 74–100%, p<0.003). Interestingly, this epimutation can be found in all cytogenetic subgroups of CLL patients and is independent of IgV(H) mutation status, making it a prime candidate for an underlying epigenetic defect in CLL. Pilot studies suggest that this epimutation regulates gene expression of the critical region via large non-coding RNA genes. In order to find out how loss of function of the 13q14 genes could result in the pathophenotype of CLL cells, we overexpressed and knocked-down RFP2, C13ORF1, KPNA3 and the largen non-coding RNA gene Dleu2 in two different cell lines and used custom oligonucleotide microarrays and timecourse experiments (n=68 array hybridizations) to identify genes that were subsequently deregulated and thus potential target genes. Less than 1% of genes represented on the arrays were significantly deregulated (median 211/25100 genes, range 44–370), showing the high specificity of the procedure. Using ingenuity pathway analyses, we found that modulation of the expression of 13q14.3 candidate genes deregulates most significantly NFkB target genes and components of the NFkB pathway itself. For a detailed validation analysis we focused on RFP2 and could show that it robustly and quickly induces NFkB activity in fibroblasts (HeLa), kidney cells (HEK-293) and CLL cell lines (Granta-591). However, analyses by oligonucleotide ELISA, Western Blot and EMSA-Band-Shift assays suggest that activation of NFkB occurs not via modulation of components of the canonical or non-canonical NFkB signalling pathways. Therefore, we propose a model for the TSM in 13q14.3 where in healthy B-cells, only one gene copy is active while the second is epigenetically silenced expression of candidate genes is deregulated in CLL cells by epimutation that is present in all cytogenetic subgroups and that this loss of function of 13q14 candidate genes results in deregulation of the NFkB signalling pathway which will change the activation level of CLL cells and their sensitivity to induction of apoptosis.

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