Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

3' UTR RNA-sequencing of humanized EGFR-mutant PC9 cell line xenografts treated with osimertinib/vehicle of RIG-I agonist IVT4/unspecific control IVT-GAC

ABSTRACT: 3' UTR RNA-sequencing of humanized EGFR-mutant PC9 cell line xenografts treated with osimertinib/vehicle of RIG-I agonist IVT4/unspecific control IVT-GAC

PROVIDER: PRJEB41855 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	ERR4972830.fastq.gz	Fastqsanger.gz
	ERR4972840.fastq.gz	Fastqsanger.gz
	ERR4972850.fastq.gz	Fastqsanger.gz
	ERR4972831.fastq.gz	Fastqsanger.gz
	ERR4972841.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 28

Similar Datasets

3' UTR RNA-sequencing of humanized EGFR-mutant PC9 cell line xenografts treated with osimertinib/vehicle of RIG-I agonist IVT4/unspecific control IVT-GAC

Project description:Immunocompromised mice were inoculated with human lung adenocarcinoma cell line PC9 and with human PBMCs. Tumors were treated with osimertinib/vehicle of RIG-I agonist IVT4/unspecific control IVT-GAC to assess response.

2021-07-20 | E-MTAB-9891 | biostudies-arrayexpress

3' UTR RNA-sequencing of human lung adenocarcinoma cell lines PC9 and A549 treated with RIG-I agonist IVT4/unspecific control IVT-GAC

Project description:The cell lines were treated with RIG-I agonist IVT4 or unspecific control IVT-GAC for 8h and then harvested for 3' UTR RNA-seq analysis

2021-08-09 | E-MTAB-10802 | biostudies-arrayexpress

Differential expression genes between PC9 cells and osimertinib resistant PC9OR cells

Project description:To investigate the possible resistant mechanism to osimertinib, PC9 cells and their derived osimertinib-resistant PC9OR cells were sequenced using illumina HiSeq. We then performed gene expression profiling analysis using data obtained from RNA-seq of PC9 cells and their derived PC9OR cells.

2022-11-02 | GSE201549 | GEO

3' UTR RNA-sequencing of human lung adenocarcinoma cell lines PC9 and A549 treated with RIG-I agonist IVT4/unspecific control IVT-GAC

Project description:3' UTR RNA-sequencing of human lung adenocarcinoma cell lines PC9 and A549 treated with RIG-I agonist IVT4/unspecific control IVT-GAC

| PRJEB46744 | ENA

scRNAseq of EGFR-mut PC9 cells control or treated for 24h or 72h with osimertinib

Project description:The experiment investigates transcriptional reponse of EGFR-mut PC9 lung cancer cells following treatment for 24h or 72h with EGFR-inhibitor osimertinib compared to control cells on a single cell level.

2021-07-19 | E-MTAB-9468 | biostudies-arrayexpress

3' UTR RNA-seq of CRISPR-edited human EGFR-mutant PC9 lung cancer cell lines after osimertinib treatment

Project description:Human EGFR-mutant lung adenocarcinoma cells (PC9) were engineered using CRISPRv2 systemt to knock-out MAVS or STING to assess impact on transcriptomic response following osimertinib treatment

2021-07-19 | E-MTAB-9885 | biostudies-arrayexpress

Gene expression of PC9 and PC9-OR cell line [JXQ_RNA]

Project description:To investigate the abnormal gene expression in Osimertinib Resistance lung cancer cell line, We performed gene expression profiling analysis using data obtained from RNA-seq of PC9 cell line and PC9-OR cell line.

2024-03-13 | GSE222820 | GEO

Gene expression profiling of drug-tolerant persister PC9 non-small cell lung cancer cells derived from osimertinib treatment

Project description:Targeting drug tolerant persister (DTP) cells may present a therapeutic opportunity to eliminate residual surviving tumor cells and impede relapse. We sought to identify therapeutically exploitable vulnerabilities in DTP cells using the EGFR-mutant non-small cell lung cancer cell line PC9 as an experimental model. Here we provide RNAseq gene expression profiling data generated from parental PC9 cells compared to PC9 DTP cells generated from nine days of treatment with 2 uM osimertinib. These data can be used to identify genes and pathways which are upregulated in DTP cells, revealing potential therapeutic targets.

2020-06-25 | GSE153183 | GEO

Single cell RNA sequencing analysis of freshly resected PC9 cell line-derived tumor xenografts

Project description:The non-small cell lung carcinoma (NSCLC) PC9 cell line is an established preclinical model for tyrosine kinase inhibitors. Using PC9 cells, we generated EGFR-mutant lung cancer xenografts to study the differences in response between individual cells and cell populations. We performed treatment of PC9 xenograft tumors with the combination of osimertinib and crizotinib as well as single drugs, followed by Drop-seq. The addition of crizotinib was guided by our previous data in PC9 grown in cell culture that identified an erlotinib-resistant drug population sensitive to crizotinib. The results of the xenograft study show that combination treatment targets specific osimertinib-tolerant cell populations but leaves a subset of the population that is tolerant to the combo. Each cell subpopulation is characterized by specific molecular signatures. The results of our study help to address emerging drug resistance that limits clinical usefulness of targeted strategies, particularly in NSCLC.

2020-12-19 | GSE160244 | GEO

SMYD5 regulates mRNA translation to promote gastric adenocarcinoma (GAC)

Project description:Dysregulated transcription due to disruption in histone lysine methylation dynamics is an established contributor to tumorigenesis. However, whether analogous pathologic epigenetic mechanisms act directly on the ribosome to advance oncogenesis is unclear. Here we find that trimethylation of the core ribosomal protein L40 at lysine 22 (rpL40K22me3) by the lysine methyltransferase (KMT) SMYD5 regulates mRNA translation output to promote gastric adenocarcinoma (GAC) malignant progression with lethal peritoneal ascites. A biochemical-proteomic strategy identifies the mono-ubiquitin fusion protein partner rpL40 as the principal physiologic substrate of SMYD5 across diverse samples. Inhibiting the SMYD5-rpL40K22me3 axis in GAC cell lines reprograms protein synthesis to attenuate oncogenic gene expression signatures. SMYD5 and rpL40K22me3 are upregulated in GAC patient samples and negatively correlate with clinical outcomes. SMYD5 ablation in vivo in familial and sporadic mouse models of malignant GAC blocks metastatic disease including peritoneal carcinomatosis (PC). Suppressing SMYD5 methylation of rpL40 inhibits human cancer cell and patient-derived GAC xenograft growth and renders them hypersensitive to PI3K/mTOR inhibitors. Finally, combining SMYD5 depletion with PI3K/mTOR inhibition and CAR-T administration cures an otherwise lethal in vivo mouse model of aggressive GAC-derived PC. Together, our work uncovers a ribosome-based epigenetic mechanism that facilitates evolution of malignant GAC and nominates SMYD5 targeting as part of a potential cornerstone combination therapy to treat a deadly cancer.

2024-03-01 | GSE238257 | 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