Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The lncRNA MIR31HG regulates the senescence associated secretory phenotype

ABSTRACT: The lncRNA MIR31HG regulates the senescence associated secretory phenotype

PROVIDER: PRJNA604779 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR11015887.fastq.gz	Fastqsanger.gz
	SRR11015888.fastq.gz	Fastqsanger.gz
	SRR11015889.fastq.gz	Fastqsanger.gz
	SRR11015890.fastq.gz	Fastqsanger.gz
	SRR11015891.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

The lncRNA MIR31HG regulates the senescence associated secretory phenotype

Project description:Oncogene-induced senescence provides a barrier against malignant transformation. Senescent cells secrete pro-inflammatory cytokines, chemokines and growth factors collectively known as the senescence-associated secretory phenotype (SASP). Paradoxically, the SASP can also negatively impact the neighbouring tissues through inducing an inflammatory environment that promotes tumorigenesis and aged-related pathologies. We have previously shown that the lncRNA MIR31HG is overexpressed and located in the cytoplasm during BRAF-induced senescence. In young proliferating cells, nuclear MIR31HG inhibits p16/CDKN2A expression through interaction with polycomb repressor complexes (PRC1/2). Here, we show that MIR31HG regulates the expression and secretion of a subset of SASP components during BRAF-induced senescence. The SASP secreted from senescent cells depleted for MIR31HG fails to induce paracrine invasion without affecting the growth inhibitory effect. Mechanistically, MIR31HG interacts with the translation factor YBX1 facilitating its phosphorylation at serine 102 (p-YBX1S102) by the kinase RSK. p-YBX1S102 induces IL1A translation which acts as upstream regulator inducing the transcription of the other SASP mRNAs. Our results suggest a dual role for MIR31HG in senescence depending on its cellular localization and place the lncRNA as a potential therapeutic target in the treatment of senescence-related pathologies.

2021-03-02 | PXD017475 | Pride

The lncRNA MIR31HG regulates the senescence associated secretory phenotype

2021-03-03 | GSE144752 | GEO

ADAM19 Mediates Cellular Senescence and the Senescence-Associated Secretory Phenotype

Project description:ADAM19 Mediates Cellular Senescence and the Senescence-Associated Secretory Phenotype

| MSV000085224 | MassIVE

Iron accumulation drives fibrosis, senescence, and the senescence-associated secretory phenotype

Project description:Iron accumulation drives fibrosis, senescence, and the senescence-associated secretory phenotype

| PRJEB62753 | ENA

Identification of the Senescence Associated Secretory Phenotype from THP-1 Monocytes

Project description:Senescence was induced in THP-1 monocytes in culture and the senescence associated secretory phenotype (SASP) was measured for the complete conditioned medium by applying nanoparticle based Proteograph technology for enrichment followed by DIA mass spectrometry

| MSV000095315 | MassIVE

MLL1 is essential for the senescence-associated secretory phenotype

Project description:MLL1 is essential for the senescence-associated secretory phenotype

| PRJNA312765 | ENA

Mettl14-driven senescence-associated secretory phenotype (SASP) facilitates somatic reprogramming

Project description:Mettl14-driven senescence-associated secretory phenotype (SASP) facilitates somatic reprogramming

| PRJNA805125 | ENA

Senescent microglia limit remyelination through the senescence associated secretory phenotype

Project description:Senescent microglia limit remyelination through the senescence associated secretory phenotype

| PRJNA1117003 | ENA

MLL1 is essential for the senescence-associated secretory phenotype

Project description:This SuperSeries is composed of the SubSeries listed below. Oncogene-induced senescence (OIS) and therapy-induced senescence (TIS), while tumor-suppressive, also promote procarcinogenic effects by activating the DNA damage response (DDR), which in turn induces inflammation. This inflammatory response prominently includes an array of cytokines known as the senescence-associated secretory phenotype (SASP). Previous observations link the transcription-associated methyltransferase and oncoprotein MLL1 to the DDR, leading us to investigate the role of MLL1 in SASP expression. Our findings reveal direct MLL1 epigenetic control over proproliferative cell cycle genes: MLL1 inhibition represses expression of proproliferative cell cycle regulators required for DNA replication and DDR activation, thus disabling SASP expression. Strikingly, however, these effects of MLL1 inhibition on SASP gene expression do not impair OIS and, furthermore, abolish the ability of the SASP to enhance cancer cell proliferation. More broadly, MLL1 inhibition also reduces âSASP-likeâ inflammatory gene expression from cancer cells in vitro and in vivo independently of senescence. Taken together, these data demonstrate that MLL1 inhibition may be a powerful and effective strategy for inducing cancerous growth arrest through the direct epigenetic regulation of proliferation-promoting genes and the avoidance of deleterious OIS- or TIS-related tumor secretomes, which can promote both drug resistance and tumor progression. Previously published samples GSM1135046, GSM1135044, GSM1135047, and GSM1135045 were also studied in this investigation and appear in GSE36641. This did not involve re-sequencing or re-alignment, nor any other deviation from the data protocols in that series. Refer to individual Series

2016-02-22 | E-GEOD-78142 | biostudies-arrayexpress

A Proteomic Atlas for the Heterogeneous Senescence Associated Secretory Phenotype

Project description:The senescence-associated secretory phenotype (SASP) has recently emerged as both a driver of -- and promising therapeutic target for -- a multitude of chronic age-related conditions, ranging from neurodegeneration to cancer. The complexity of the SASP, typically monitored by the secretion of a few proteins, has been greatly underappreciated, and a small set of factors cannot explain the diverse phenotypes it produces in vivo. Here, we present SASP Atlas, a comprehensive proteomic database of SASPs driven by multiple inducers of senescence in different human cell types. While there are common elements among all the SASPs we have documented so far, we discovered distinct senescence inducer- and cell type-specific secretory proteins. In all cases, the SASPs are comprised of hundreds of unique proteins secreted as both soluble proteins (sSASP) and exosomes (eSASP) with distinct and novel protein profiles. This resource will aid in identifying the proteins that drive senescence-associated phenotypes and provide comprehensive catalogs of potential senescence biomarkers that can be used to assess the burden and the originating stimuli and type of senescent cells in vivo.

2019-02-21 | MSV000083468 | MassIVE

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