Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

MYCN drives chemoresistance in small cell lung cancer while USP7 inhibition can restore chemosensitivity

ABSTRACT: MYCN drives chemoresistance in small cell lung cancer while USP7 inhibition can restore chemosensitivity

PROVIDER: PRJNA682599 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR13198900.fastq.gz	Fastqsanger.gz
	SRR13198901.fastq.gz	Fastqsanger.gz
	SRR13198902.fastq.gz	Fastqsanger.gz
	SRR13198903.fastq.gz	Fastqsanger.gz
	SRR13198904.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 21

Similar Datasets

MYCN drives chemoresistance in small cell lung cancer while USP7 inhibition can restore chemosensitivity [tumor]

Project description:MYCN drives chemoresistance in small cell lung cancer while USP7 inhibition can restore chemosensitivity [tumor]

| PRJNA682606 | ENA

MYCN drives chemoresistance in small cell lung cancer while USP7 inhibition can restore chemosensitivity [cells]

Project description:MYCN drives chemoresistance in small cell lung cancer while USP7 inhibition can restore chemosensitivity [cells]

| PRJNA682605 | ENA

MYCN drives chemoresistance in small cell lung cancer while USP7 inhibition can restore chemosensitivity [cells]

Project description:This study assessed gene expression in mouse SCLC with inducible MYCN overexpression

2020-12-05 | GSE162679 | GEO

MYCN drives chemoresistance in small cell lung cancer while USP7 inhibition can restore chemosensitivity [tumor]

Project description:This study assessed gene expression in mouse SCLC with inducible MYCN overexpression in tumors

2020-12-05 | GSE162680 | GEO

<i>MYCN</i> drives chemoresistance in small cell lung cancer while USP7 inhibition can restore chemosensitivity.

Project description:Small cell lung cancer (SCLC) is an aggressive neuroendocrine cancer characterized by initial chemosensitivity followed by emergence of chemoresistant disease. To study roles for MYCN amplification in SCLC progression and chemoresistance, we developed a genetically engineered mouse model of MYCN-overexpressing SCLC. In treatment-naïve mice, MYCN overexpression promoted cell cycle progression, suppressed infiltration of cytotoxic T cells, and accelerated SCLC. MYCN overexpression also suppressed response to cisplatin-etoposide chemotherapy, with similar findings made upon MYCL overexpression. We extended these data to genetically perturb chemosensitive patient-derived xenograft (PDX) models of SCLC. In chemosensitive PDX models, overexpression of either MYCN or MYCL also conferred a switch to chemoresistance. To identify therapeutic strategies for MYCN-overexpressing SCLC, we performed a genome-scale CRISPR-Cas9 sgRNA screen. We identified the deubiquitinase USP7 as a MYCN-associated synthetic vulnerability. Pharmacological inhibition of USP7 resensitized chemoresistant MYCN-overexpressing PDX models to chemotherapy in vivo. Our findings show that MYCN overexpression drives SCLC chemoresistance and provide a therapeutic strategy to restore chemosensitivity.

| S-EPMC7462062 | biostudies-literature

MYCN drives chemoresistance in small cell lung cancer while USP7 inhibition can restore chemosensitivity

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

2020-12-05 | GSE162681 | GEO

Microarry from Treg with conditional knockout of Usp7

Project description:Microarry from Treg with conditional knockout of Usp7 RNA from three independent samples from FACS sorted CD4+YFP+ Treg of fl-Usp7/Foxp3cre mice, compared to Foxp3cre control (C57BL/6 background).

2015-09-15 | E-GEOD-72988 | biostudies-arrayexpress

Phase separation of RXRγ drives tumor chemoresistance and represents a therapeutic target for small cell lung cancer

Project description:Small cell lung cancer (SCLC) is the most lethal type of lung cancer, characterized by limited treatment options and rapid evolution from chemosensitivity to chemoresistance. However, the mechanisms underlying this evolution remain poorly understood. Identifying the druggable drivers and developing pharmacological strategies to overcome chemoresistance are imperative. Here, we show that Retinoid X receptor γ (RXRγ) is uniquely overexpressed in chemo-resistant SCLC tumors, and that RXRγ serves as an essential factor driving chemoresistance in SCLC. RXRγ forms phase-separated droplets with LSD1 in the nucleus, which enhances RXRγ-mediated gene transcription activity and reprograms gene expression, promoting tumor stemness and metastasis, and eventually driving SCLC chemoresistance. In turn, RXRγ antagonist disrupts RXRγ-LSD1 interaction, reducing their binding to the target gene locus, markedly suppressing the expression of the RXRγ target gene network. Finally, RXRγ antagonists strongly suppress tumor growth and metastasis and restore SCLC vulnerability to chemotherapy in multiple preclinical SCLC models, without overt toxicity, in mice. Thus, these results establish RXRγ as a key player in SCLC by phase separation and as a potential therapeutic target for this deadly disease.

2024-12-31 | GSE269090 | GEO

Phase separation of RXRγ drives tumor chemoresistance and represents a therapeutic target for small cell lung cancer

2024-12-31 | GSE277738 | GEO

YG001: A Usp7-Tip60 pathway regulates early adipogenesis

Project description:USP7, a dominant DUB activity in 3T3-L1 adipocytes and in mouse adipose tissue, increases Tip60 protein levels, and deubiquitinates Tip60 both in intact cells and in vitro. Treatment with a pan deubiquitinase (DUB) inhibitor, or knockdown of USP7, decreases adipogenesis. Transcriptome analysis reveals a common set of cell cycle genes to be co-regulated by both Tip60 and USP7. Knock down of either factor results in impaired mitotic clonal expansion, an early step in adipogenesis. These results therefore reveal deubiquitination of a transcriptional coregulator to be a key mechanism in the regulation of early adipogenesis Mature 3T3-L1 adipocytes were subjected to RNAi-mediated knock down with control(C), USP7(U)- or Tip60(T)-specific oligonucleotides. For this, 4 replicates of differentiated 3T3-L1 cells were transfected with Amaxa technology. Two days after transfection cells were washed twice with PBS twice and lysed in 0.5ml Trizol (Invitrogen). mRNA expression of Tip60 and USP7 was assessed by qRT-PCR. Amplified cRNA samples were labeled with either cy3 or cy5 and put on microarray together with and oppositely labeled common reference sample consisting of cRNA derived from undifferentiated 3T3-L1 cells.

2013-08-28 | E-GEOD-28587 | biostudies-arrayexpress

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