The molecular dynamics of long noncoding RNA control of transcription in PTEN and its pseudogene

Lister, Nicholas C.; Shevchenko, Galina; Walshe, J.L.; Groen, Jessica N.; Johnsson, Per; Vidarsdóttir, Linda; Grandér, Dan; Ataide, Sandro F.; Morris, Kevin V.

doi:10.1073/pnas.1621490114

Cited by 35 publications

(33 citation statements)

References 18 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…ATP is a required substrate for serine/threonine kinase (ATM) phosphorylation of histones (Banerjee, Bennion, Goldberg, & Allen, 1991), which is removed by protein serine/threonine phosphatases (PSPs) 2013). Additionally, lncRNAs can act as sRNA sponges and stabilize mRNA Lister et al, 2017). As previously stated, lncRNA can also guide nucleosome remodeling proteins to targeted genomic regions (Tang et al, 2017).…”

Section: Rna-mediated Chromatin Regulationmentioning

confidence: 91%

“…LncRNAs can guide both histones modifying proteins and DNA methyltransferases to targeted sites on the chromosome, which can give these proteins loci specificity (O’Leary et al, 2017) (reviewed in (Mercer & Mattick, 2013)). Additionally, lncRNAs can act as sRNA sponges and stabilize mRNA (Du et al, 2016; Lister et al, 2017). As previously stated, lncRNA can also guide nucleosome remodelling proteins to targeted genomic regions (Y.…”

Section: Chromatin and Gene Regulationmentioning

confidence: 99%

See 1 more Smart Citation

Chromatin modifications in metabolic disease: Potential mediators of long‐term disease risk

Costello

Schones

2018

WIREs Mechanisms of Disease

View full text Add to dashboard Cite

Metabolic diseases such as obesity and diabetes are complex diseases resulting from multiple genetic and environmental factors, such as diet and activity levels. These factors are well known contributors to the development of metabolic diseases. One manner by which environmental factors can influence metabolic disease progression is through modifications to chromatin. These modifications can lead to altered gene regulatory programs, which alters disease risk. Furthermore, there is evidence that parents exposed to environmental factors can influence the metabolic health of offspring, especially if exposures are during intrauterine growth periods. In this Review, we outline the evidence that chromatin modifications are associated with metabolic diseases, including diabetes and obesity. We also consider evidence that these chromatin modifications can lead to long-term disease risk and contribute to disease risk for future generations.

show abstract

Section: Rna-mediated Chromatin Regulationmentioning

confidence: 91%

Section: Chromatin and Gene Regulationmentioning

confidence: 99%

Chromatin modifications in metabolic disease: Potential mediators of long‐term disease risk

Costello

Schones

2018

WIREs Mechanisms of Disease

View full text Add to dashboard Cite

show abstract

“…PTENP1 asRNA α binds the PTEN promoter, and epigenetically downregulates PTEN transcription by the recruitment of DNMT3a and Enhancer of zeste homolog 2 (EZH2) to enhance the methylation of PTEN promoter. PTENP1 asRNA α knockdown induces cell cycle arrest and sensitizes cells to doxorubicin, suggesting the biological function for the PTENP1 asRNAs [ 133 , 136 ].…”

Section: Lncrnas Modulate Pten Expression Indirectlymentioning

confidence: 99%

Regulation of PTEN expression by noncoding RNAs

Zhang

Guo

et al. 2018

J Exp Clin Cancer Res

View full text Add to dashboard Cite

Phosphatase and tensin homologue (PTEN) triggers a battery of intracellular signaling pathways, especially PI3K/Akt, playing important roles in the pathogenesis of multiple diseases, such as cancer, neurodevelopmental disorders, cardiovascular dysfunction and so on. Therefore PTEN might be a biomarker for various diseases, and targeting the abnormal expression level of PTEN is anticipated to offer novel therapeutic avenues. Recently, noncoding RNAs (ncRNAs) have been reported to regulate protein expression, and it is definite that PTEN expression is controlled by ncRNAs epigenetically or posttranscriptionally as well. Herein, we provide a review on current understandings of the regulation of PTEN by ncRNAs, which could contribute to the development of novel approaches to the diseases with abnormal expression of PTEN.

show abstract

“…Most of human non-coding RNA (ncRNA) transcripts do not code for protein products, but an increasing number of ncRNAs are identi ed to be functional and important in biological or pathological processes [1]. Accumulated evidence suggested that abnormal expression of lncRNAs is often associated with disease pathology especially tumors through microRNA or protein function regulation [2]. Several types of lncRNAs are identi ed as modulating RNAs which possess orchestrated functions involved in the control of genome dynamics, cell biology, and tumor developmental programming [3][4][5].…”

Section: Introductionmentioning

confidence: 99%

The Sulfatide/Myb/MEF2C Axis Controls the Malignant Behaviors of Hepatocellular Carcinoma Cells by Modulating lncAY Expression

Chen

Cai

et al. 2020

Preprint

View full text Add to dashboard Cite

Background: Long noncoding RNA (lncRNA) is often abnormally expressed in tumors especially hepatocellular carcinoma (HCC) and involved in tumor progression. However, the dysregulation of lncRNA expression in tumors is poorly understood. Methods: The expression of lncRNA was determined and screened by microarray, RT-PCR, qPCR and in situ hybridization in HCC cells. Multiple component transcription analysis, dual-luciferase reporter assays and chromatin immunoprecipitation were performed to investigate transcriptional regulation of the lncRNA expression. Co-immunoprecipitation, point mutation and western blots were carried out for the analysis of acetylation regulation.Results: Here, we showed that lncRNA AY927503 (lncAY) was regulated in HCC cells by sulfatide-mediated transcriptional axis. Sulfatide significantly strengthened lncAY expression and promoted HCC cell migration, proliferation or angiogenesis, whereas cerebroside sulfotransferase silence reduced lncAY expression and drastically hindered HCC cell proliferation, migration or angiogenesis. Interestingly, sulfatide significantly enhanced the activity of reporter carrying lncAY gene promoter. Myb and MEF2C were then identified as the transcription factors responsive to sulfatide and responsible for the stimulation of lncAY promoter activity and lncAY transcription. Both Myb and MEF2C enrichment on lncAY promoter was further confirmed in HCC cells, and their occupancy on lncAY promoter was enhanced by sulfatide for Myb or MEF2C was acetylated. However, Myb mutation of K456/503A prevented Myb from being acetylated under the induction by sulfatide, and the mutant Myb K456/503A was unable to occupy lncAY promoter and enhance lncAY transcription. Myb or MEF2C was complexed with SIN3B or p300. In the presence of sulfatide, HDAC2 dissociation from SIN3B complex was observed. Conclusion: These results uncovered the sulfatide/Myb/MEF2C/lncAY axis in HCC, which controls HCC cell proliferation, and provided an insight into the mechanisms of lncAY dysregulation.

show abstract

The molecular dynamics of long noncoding RNA control of transcription in PTEN and its pseudogene

Cited by 35 publications

References 18 publications

Chromatin modifications in metabolic disease: Potential mediators of long‐term disease risk

Chromatin modifications in metabolic disease: Potential mediators of long‐term disease risk

Regulation of PTEN expression by noncoding RNAs

The Sulfatide/Myb/MEF2C Axis Controls the Malignant Behaviors of Hepatocellular Carcinoma Cells by Modulating lncAY Expression

Contact Info

Product

Resources

About