Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Long non-coding RNA TINCR suppresses metastatic melanoma dissemination by preventing ATF4 translation

ABSTRACT: Long non-coding RNA TINCR suppresses metastatic melanoma dissemination by preventing ATF4 translation

PROVIDER: PRJNA517668 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR4033030_1.fastq.gz	Fastqsanger.gz
	SRR4033030_2.fastq.gz	Fastqsanger.gz
	SRR4033040_1.fastq.gz	Fastqsanger.gz
	SRR4033040_2.fastq.gz	Fastqsanger.gz
	SRR4033050_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 96

Similar Datasets

Long non-coding RNA TINCR suppresses metastatic melanoma dissemination by preventing ATF4 translation.

Project description:Transition from proliferative-to-invasive phenotypes promotes metastasis and therapy resistance in melanoma. Reversion of the invasive phenotype, however, is challenged by the poor understanding of mechanisms underlying its maintenance. Here, we report that the lncRNA TINCR is down-regulated in metastatic melanoma and its silencing increases the expression levels of invasive markers, in vitro migration, in vivo tumor growth, and resistance to BRAF and MEK inhibitors. The critical mediator is ATF4, a central player of the integrated stress response (ISR), which is activated in TINCR-depleted cells in the absence of starvation and eIF2α phosphorylation. TINCR depletion increases global protein synthesis and induces translational reprogramming, leading to increased translation of mRNAs encoding ATF4 and other ISR proteins. Strikingly, re-expression of TINCR in metastatic melanoma suppresses the invasive phenotype, reduces numbers of tumor-initiating cells and metastasis formation, and increases drug sensitivity. Mechanistically, TINCR interacts with mRNAs associated with the invasive phenotype, including ATF4, preventing their binding to ribosomes. Thus, TINCR is a suppressor of the melanoma invasive phenotype, which functions in nutrient-rich conditions by repressing translation of selected ISR RNAs.

| S-EPMC7926219 | biostudies-literature

Long non-coding RNA TINCR suppresses metastatic melanoma dissemination by preventing ATF4 translation

Project description:Transition from proliferative to invasive phenotypes promotes metastasis and therapy resistance in melanoma. Reversion of the invasive phenotype, however, is challenged by the poor understanding of mechanisms underlying its maintenance. Here, we report that the lncRNA TINCR is down-regulated in metastatic melanoma and its silencing increases the expression levels of invasive markers, in vitro migration, in vivo tumor growth and resistance to BRAF- and MEK-inhibitors. The critical mediator is ATF4, a central player of the integrated stress response (ISR), which is activated in TINCR-depleted cells in the absence of starvation and eIF2? phosphorylation. TINCR depletion increases global protein synthesis and induces translational reprogramming, leading to increased translation of mRNAs encoding ATF4 and other ISR proteins. Strikingly, re-expression of TINCR in metastatic melanoma suppresses the invasive phenotype, reduces numbers of tumor-initiating cells and metastasis formation, and increases drug sensitivity. Mechanistically, TINCR interacts with mRNAs associated with the invasive phenotype, including ATF4, preventing their binding to ribosomes. Thus, TINCR is a suppressor of the melanoma invasive-phenotype, which functions in nutrient-rich conditions by repressing translation of selected ISR RNAs.

| S-SCDT-EMBOR-2020-50852-T | biostudies-other

Long non-coding RNA TINCR suppresses metastatic melanoma dissemination by preventing ATF4 translation

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-11-25 | GSE125835 | GEO

lncRNA TINCR antisense pulldown of interacting RNAs

Project description:Purpose: Identify RNA interactome of lncRNA TINCR Methods: Primary melanoma cell lines WM902B and MMC70 lysates hybridized with TINCR antisense DNA oligos Results: we found that TINCR silencing induces activation of translation of ATF4 and other stress responsive RNAs.

2020-11-25 | GSE125833 | GEO

Ribosome profiling analysis of lncRNA TINCR silenced primary melanoma cell line WM902B

Project description:Purpose: Study the changes in mRNA translation upon silencing of lncRNA TINCR Methods: Primary melanoma cell line WM902B was transduced with lientiviruses expressing Scrambled and TINCR directed shRNA hairpins Results: we found that TINCR silencing induces activation of ATF4 translation

2020-11-25 | GSE125832 | GEO

RNAseq analysis of MM13 and MM2 metastatic melanoma PDX cells overexpressing TINCR

Project description:Purpose: Study the changes in cell transcriptome upon overexpression of lncRNA TINCR Methods: Primary melanoma cell line WM902B was transduced with lientiviruses expressing Scrambled and TINCR directed shRNA hairpins Results: we found that TINCR overexpression induces partial reversion of invasive phenotype

2020-11-25 | GSE125834 | GEO

Tincr

Project description:Mus musculus Tincr, TINCR ubiquitin domain containing [Source:MGI Symbol;Acc:MGI:5012404], is differentially expressed in 21 experiment(s);

| ENSMUSG00000110218 | ExpressionAtlas

TINCR

Project description:Homo sapiens TINCR, TINCR ubiquitin domain containing [Source:HGNC Symbol;Acc:HGNC:14607], is differentially expressed in 107 experiment(s);

| ENSG00000223573 | ExpressionAtlas

TINCR

Project description:Homo sapiens TINCR, TINCR ubiquitin domain containing [Source:HGNC Symbol;Acc:HGNC:14607], is expressed in 33 baseline experiment(s);

| ENSG00000223573 | ExpressionAtlas

Tincr

Project description:Mus musculus Tincr, TINCR ubiquitin domain containing [Source:MGI Symbol;Acc:MGI:5012404], is expressed in 33 baseline experiment(s);

| ENSMUSG00000110218 | ExpressionAtlas

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