Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

CircPOLA2 sensitizes NSCLC cells to ferroptosis and suppresses tumorigenesis via the Merlin-YAP signaling pathway

ABSTRACT: CircPOLA2 sensitizes NSCLC cells to ferroptosis and suppresses tumorigenesis via the Merlin-YAP signaling pathway

PROVIDER: PRJNA1070253 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR27749132_1.fastq.gz	Fastqsanger.gz
	SRR27749132_2.fastq.gz	Fastqsanger.gz
	SRR27749133_1.fastq.gz	Fastqsanger.gz
	SRR27749133_2.fastq.gz	Fastqsanger.gz
	SRR27749134_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 16

Similar Datasets

CircPOLA2 sensitizes NSCLC cells to ferroptosis and suppresses tumorigenesis via the Merlin-YAP signaling pathway

Project description:Circular RNAs (circRNAs) have been implicated in the tumorigenesis of non-small cell lung cancer (NSCLC). Ferroptosis is considered a mechanism to suppress tumorigenesis. Herein, we identified a novel downregulated circRNA, circPOLA2 (hsa_circ_0004291), in NSCLC tissues and found that it was correlated with advanced clinical stage in patients. Nuclear-cytoplasmic fractionation assays and FISH assays confirmed that circPOLA2 was predominantly localized in the cytoplasm. Overexpression of circPOLA2 promoted lipid peroxidation and ferroptosis in NSCLC cells, thereby inhibiting cell proliferation and migration, while knockdown of circPOLA2 exerted the opposite effects. Mechanistically, circPOLA2 interacted with Merlin, a critical regulator of the Hippo pathway, and restricted Merlin phosphorylation at S518, leading to the activation of the Hippo pathway. In addition, circPOLA2 enhanced ferroptosis in NSCLC cells by activating the Hippo pathway. Together, circPOLA2 sensitizes cells to ferroptosis and suppresses tumorigenesis in NSCLC by facilitating Merlin-mediated activation of the Hippo signaling pathway.

2024-08-20 | GSE254362 | GEO

Inhibiting LCN2 can suppress the development of NSCLC by promoting ferroptosis

Project description:Ferroptosis, a recently discovered form of regulated cell death, has been closely linked to tumor progression. However, the underlying mechanism of ferroptosis in non-small cell lung cancer (NSCLC) remains unclear. In this study, we conducted transcriptome sequencing on NSCLC samples. Overall, our study suggests that suppressing LCN2 can effectively inhibit the development of NSCLC by promoting ferroptosis

2023-07-27 | GSE238161 | GEO

MYCN mediates cysteine addiction and sensitizes to ferroptosis

Project description:MYCN mediates cysteine addiction and sensitizes to ferroptosis

| PRJNA781844 | ENA

YAP/TAZ and ATF4 collaboratively drive resistance to Sorafenib therapy in hepatocellular carcinoma by preventing ferroptosis

Project description:Understanding the mechanisms underlying evasive resistance in cancer is an unmet medical need to improve the efficacy of current therapies. In this study, a combination of shRNA-mediated synthetic lethality screening and transcriptomic analysis revealed the transcription factors YAP/TAZ as key drivers of Sorafenib resistance in hepatocellular carcinoma (HCC) by repressing Sorafenib-induced ferroptosis. Mechanistically, in a TEAD-dependent manner YAP/TAZ induce the expression of SLC7A11, a key transporter maintaining intracellular glutathione homeostasis, thus enabling HCC cells to overcome Sorafenib-induced ferroptosis. At the same time, YAP/TAZ sustain the protein stability, nuclear localization and transcriptional activity of ATF4 which in turn cooperates to induce SLC7A11 expression. Our study uncovered a critical role of YAP/TAZ in the repression of ferroptosis and thus in the establishment of Sorafenib resistance in HCC, highlighting YAP/TAZ-based rewiring strategies as potential approaches to overcome HCC therapy resistance.

2021-08-20 | GSE181771 | GEO

Gene expression changes caused by YAP overexpression and Nf2 deletion in the developing mouse brain

Project description:The transcriptional coactivator YAP is the key downstream effector of the Hippo pathway. YAP overexpression in the developing mouse brain results in excessive expansion of the neural progenitor pool and severe perturbation of brain development. Nf2/Merlin is a tumor suppressor whose mutations are found in many human cancers. Loss of Merlin during brain development causes overexpansion of the neural progenitor pool. We used microarrays to identify the gene expression changes caused by YAP overexpression and Nf2 deletion. We used a double-transgenic system to overexpress YAP in the developing mouse brain by crossing mice carrying a doxycycline-dependent allele of YAP1-S127A (TetO-YAP1) with those expressing the reverse tetracycline-dependent transactivator rtTA under the control of the neural progenitor-specific Nestin promoter (Nes-rtTA) and feeding the dam with doxycycline-containing food (200 mg/kg) from E7.5. We conditionally deleted Nf2 using the telencephalon-specific Emx1-Cre.

2013-06-19 | E-GEOD-48078 | biostudies-arrayexpress

MYCN mediates cysteine addiction and sensitizes neuroblastoma to ferroptosis

Project description:MYCN mediates cysteine addiction and sensitizes neuroblastoma to ferroptosis

| PRJNA793984 | ENA

Gene expression changes caused by YAP overexpression and Nf2 deletion in the developing mouse brain

2013-06-19 | GSE48078 | GEO

BRD4 inhibition sensitizes diffuse large B-cell lymphoma cells to ferroptosis

Project description:BRD4 inhibition sensitizes diffuse large B-cell lymphoma cells to ferroptosis

| PRJNA970029 | ENA

Inhibiting LCN2 can suppress the development of NSCLC by promoting ferroptosis

Project description:Inhibiting LCN2 can suppress the development of NSCLC by promoting ferroptosis

| PRJNA998065 | ENA

BRD4 inhibition sensitizes diffuse large B-cell lymphoma cells to ferroptosis

Project description:Diffuse large B-cell lymphoma (DLBCL), the most common form of non-Hodgkin lymphoma, is characterized by an aggressive clinical course. In approximately one-third of DLBCL patients, first-line multi-agent immunochemotherapy fails to produce a durable response. Molecular heterogeneity and apoptosis resistance pose major therapeutic challenges in DLBCL treatment. To circumvent apoptosis resistance, the induction of ferroptosis might represent a promising strategy for lymphoma therapy. Here, a compound library targeting epigenetic modulators was screened to identify ferroptosis-sensitizing drugs. Strikingly, bromodomain and extra-terminal domain (BET) inhibitors sensitized cells of the germinal center B cell-like (GCB) subtype of DLBCL to ferroptosis induction and the combination of BET inhibitors with ferroptosis inducers, such as dimethyl fumarate (DMF) or RSL3, synergized in the killing of DLBCL cells in vitro and in vivo. On the molecular level, the BET protein BRD4 was found to be an essential regulator of ferroptosis suppressor protein 1 (FSP1) expression and to thus protect GCB DLBCL cells from ferroptosis. Collectively, we identified and characterized BRD4 as an important player in ferroptosis suppression in GCB DLBCL and provide a rationale for the combination of BET inhibitors with ferroptosis-inducing agents as a novel therapeutic approach for DLBCL treatment.

2023-08-01 | GSE231871 | 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