Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Evaluation of the interplay between the ADAR editome and immunotherapy in melanoma

ABSTRACT: We evaluated the editome of melanoma cell lines generated from patients pre- and post-immunotherapy with immune checkpoint inhibitors by RNAseq. Our results reveal a differential editing in Alu sequences between samples pre-therapy and relapses during therapy with immune checkpoint inhibitors

ORGANISM(S): Homo sapiens

PROVIDER: GSE162095 | GEO | 2020/11/25

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Evaluation of the Interplay between the ADAR Editome and Immunotherapy in Melanoma.

Project description:BackgroundRNA editing is a highly conserved posttranscriptional mechanism that contributes to transcriptome diversity. In mammals, it includes nucleobase deaminations that convert cytidine (C) into uridine (U) and adenosine (A) into inosine (I). Evidence from cancer studies indicates that RNA-editing enzymes promote certain mechanisms of tumorigenesis. On the other hand, recoding editing in mRNA can generate mutations in proteins that can participate in the Major Histocompatibility Complex (MHC) ligandome and can therefore be recognized by the adaptive immune system. Anti-cancer treatment based on the administration of immune checkpoint inhibitors enhance these natural anti-cancer immune responses.ResultsBased on RNA-Seq datasets, we evaluated the editome of melanoma cell lines generated from patients pre- and post-immunotherapy with immune checkpoint inhibitors. Our results reveal a differential editing in Arthrobacter luteus (Alu) sequences between samples pre-therapy and relapses during therapy with immune checkpoint inhibitors.ConclusionThese data pave the way towards the development of new diagnostics and therapies targeted to editing that could help in preventing relapses during immunotherapies.

| S-EPMC7838980 | biostudies-literature

Evaluation of the interplay between the ADAR editome and immunotherapy in melanoma

Project description:Evaluation of the interplay between the ADAR editome and immunotherapy in melanoma

| PRJNA680560 | ENA

The C. elegans neural editome reveals an ADAR target mRNA required for proper chemotaxis

Project description:ADAR proteins alter gene expression both via catalyzing adenosine-to-inosine RNA editing and in an editing-independent manner by binding to target RNAs. Loss of ADARs affects neuronal function in all animals studied to date. To identify important neuronal targets in C. elegans, we performed the first unbiased assessment of the effects of ADR-2, the C. elegans editing enzyme, on the neural transcriptome. We identified the neural editome and gene expression changes associated with the loss of adr-2. As C. elegans lacking adr-2 exhibit reduced chemotaxis, our studies focused on targets that regulate this process. We identified an edited mRNA, clec-41, whose expression is dependent on ADR-2. Expressing clec-41 in adr-2 deficient neural cells restored chemotaxis. This study is the first of its kind in the RNA editing field to span from developing novel methodology for tissue-specific target identification to organismal behavior, significantly advancing our understanding of ADAR functions in neural cells.

2017-06-13 | GSE98869 | GEO

The landscape of A-to-I RNA editome in mouse embryonic development

Project description:A-to-I editing, as a post-transcriptional modification process mediated by ADAR, plays a crucial role in many biological process in metazoans.The study of RNA editing in mouse early embryonic development can understand the dynamic changes of RNA editing during mouse early embryonic development, and further reveal the role of RNA editing in mouse early embryo development.We found that as embryonic developing, RNA editome in mice is getting more and more. Besides, RNA editome in mouse embryonic development is stage specified.

2018-11-28 | GSE123012 | GEO

The C. elegans neural editome reveals an ADAR target mRNA required for proper chemotaxis.

Project description:ADAR proteins alter gene expression both by catalyzing adenosine (A) to inosine (I) RNA editing and binding to regulatory elements in target RNAs. Loss of ADARs affects neuronal function in all animals studied to date. Caenorhabditis elegans lacking ADARs exhibit reduced chemotaxis, but the targets responsible for this phenotype remain unknown. To identify critical neural ADAR targets in C. elegans, we performed an unbiased assessment of the effects of ADR-2, the only A-to-I editing enzyme in C. elegans, on the neural transcriptome. Development and implementation of publicly available software, SAILOR, identified 7361 A-to-I editing events across the neural transcriptome. Intersecting the neural editome with adr-2 associated gene expression changes, revealed an edited mRNA, clec-41, whose neural expression is dependent on deamination. Restoring clec-41 expression in adr-2 deficient neural cells rescued the chemotaxis defect, providing the first evidence that neuronal phenotypes of ADAR mutants can be caused by altered gene expression.

| S-EPMC5644944 | biostudies-literature

The landscape of A-to-I RNA editome from 462 individuals human genomes

Project description:A-to-I editing, as a post-transcriptional modification process mediated by ADAR, plays a crucial role in many biological process in metazoans. However, how and to what extent that A-to-I editing diversifies and shapes the population diversity at the RNA level is largely unknown. We employed 462 mRNA-sequencing data from five populations of the Geuvadis Project and identified 16,518 A-to-I editing sites, forming a landscape of RNA editome of the human genome. By exploration of RNA editing within and between populations, we discovered non-adaption of nonsynonymous editing in the evolution, and revealed geographic restriction of rare editing sites. Moreover, we showed that RNA editing can characterize the subtle but substantial divergence between different populations, especially those from different continents. Altogether, we demonstrated RNA editing can well depict the nature and structure of populations at RNA level, which provides insights into the process of how A-to-I editing shapes population diversity at transcriptomic level. Our work will facilitate the understanding of the landscape of RNA editome at population-scale, and be helpful to interpret difference in the distribution and prevalence of disease among individuals and across populations.

2017-08-31 | GSE103294 | GEO

DNA Methylation Inhibitors in Immunotherapy

Project description:<p>We show that DNA methyltransferase inhibitors (DNMTis) upregulate immune signaling in cancer through the viral defense pathway and re-expression of epigenetically silenced endogenous retrovirus. In melanoma patients treated with an immune checkpoint therapy, high viral defense signature expression in tumors significantly associates with durable clinical response and DNMTi treatment sensitizes to anti-CTLA4 therapy in a pre-clinical melanoma model.</p>

| phs001038 | dbGaP

Suppression of adenosine-to-inosine (A-to-I) RNA editome by death associated protein 3 (DAP3) promotes cancer progression

Project description:RNA editing introduces nucleotide changes in RNA sequences. Recent studies have reported that aberrant A-to-I RNA editing profiles are implicated in cancers. Albeit changes in expression and activity of ADAR genes are thought to have been responsible for the dysregulated RNA editome in diseases, they are not always correlated, indicating the involvement of secondary regulators. Here, we uncover DAP3 as a potent repressor of editing and a strong oncogene in cancer. DAP3 mainly interacts with the deaminase domain of ADAR2 and represses editing via disrupting association of ADAR2 with its target transcripts. PDZD7, an exemplary DAP3-repressed editing target, undergoes a protein recoding editing at stop codon [Stop →Trp (W)]. Because of editing suppression by DAP3, the unedited PDZD7WT, which is more tumorigenic than edited PDZD7Stop518W, is accumulated in tumors. In sum, cancer cells may acquire malignant properties for their survival advantage through suppressing RNA editome by DAP3.

2020-06-23 | GSE123020 | GEO

Placental Editome Profiling Reveals Widespread RNA-Editing Dysregulation in Preeclampsia

Project description:Placental Editome Profiling Reveals Widespread RNA-Editing Dysregulation in Preeclampsia

| PRJNA623568 | ENA

Placental Editome Profiling Reveals Widespread RNA-Editing Dysregulation in Preeclampsia

Project description:Dysregulated RNA editing is well documented in several diseases such as cancer. The extent to which RNA editing might be involved in diseases originated in the placenta such as preeclampsia remains unknown, because RNA editing has rarely been studied in the placenta. Here, the RNA editome is systematically profiled on placentae from 9 patients with early-onset severe preeclampsia (EOSPE) and 32 normal controls, and a widespread RNA editing dysregulation in EOSPE has been identified. The mis-edited gene set is enriched with known preeclampsia-associated genes and differentially expressed genes in EOSPE. The “RNA editing events” at two microRNA binding sites in 3’-UTR of the LEP mRNA have been generated, which leads to increased expression level of LEP in trophoblast cells. Upregulation of LEP is also observed in the placentae of PE patients. These results suggest that widespread placental RNA editing may be involved in placental development and dysregulation of RNA editing in the placenta may contribute to the pathogenesis of preeclampsia.

2020-04-20 | GSE148241 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data