Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNAseq of parental and persister cells generated human cancer cells

ABSTRACT: RNAseq of parental and persister cells generated human cancer cells

PROVIDER: PRJNA783910 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR17048100_1.fastq.gz	Fastqsanger.gz
	SRR17048100_2.fastq.gz	Fastqsanger.gz
	SRR17048101_1.fastq.gz	Fastqsanger.gz
	SRR17048101_2.fastq.gz	Fastqsanger.gz
	SRR17048102_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 182

Similar Datasets

Parental and persister cells generated human cancer cells

Project description:Parental and persister cells generated human cancer cells

| PRJNA783928 | ENA

RNAseq of parental and persister cells generated human cancer cells

Project description:Persister cells (PS) were generated by diverse drug treatments of PC9 cells. Transcriptomes of these differently generated drug-persisting cells revealed common gene expression signatures related to metastasis and invasion. To test the impact of ATF4 and BCL2 effector proteins on the gene expression profiles of PS, we also investigated changes in gene expression upon BH3-mimetic treatment after gene knock-down. Enrichment analysis of differentially expressed genes (DEGs) confirmed the overall dependence on BCl-2 effector proteins and ATF4 for our previously identified pathways.

2022-09-06 | GSE189625 | GEO

A375 melanoma parental and persister cells

Project description:A375 melanoma parental and persister cells

| PRJNA566394 | ENA

scRNAseq of PC9 parental and persister cells

Project description:scRNAseq of PC9 parental and persister cells

| PRJNA783931 | ENA

Expression data from A375 melanoma parental and persister cells

Project description:Identify transcriptionnally and translationally regulated mRNA in melanoma parental and persister cells In this dataset, we include expression data of A375 melanoma drug-naïve parental cells and A375 melanoma persister cells that survived from BRAF and MEK inhibition. The expression data are studied in both total RNA and polysome-bounded RNA.

2019-09-20 | GSE137724 | GEO

scRNAseq of PC9 parental and persister cells

Project description:We performed scRNAseq of PC9 parental (PT) and persister cells (PS) at d1, d3 and d7 after being generated by treatment with BH3-mimetics. Trajectory analysis and differential expression along the pseudotime revealed the upregulation of the integrated stress response (ISR) and EMT signatures at early pseudotime, while gene expression profiles for cell cycle progression were upregulated at late pseudotime, characteristic for late PS and PT.

2022-09-06 | GSE189638 | GEO

m6A-seq of melanoma parental and persister cells

Project description:We study the m6A distribution on mRNAs from melanoma drug-naïve parental and persister cells treated with BRAF and MEK inhibitors.

2019-09-20 | GSE137725 | GEO

m6A-seq of melanoma parental and persister cells

Project description:m6A-seq of melanoma parental and persister cells

| PRJNA566396 | ENA

Gene expression profiling of drug-tolerant persister BT474 breast cancer cells derived from lapatinib treatment

Project description:Acquired drug resistance prevents targeted cancer therapy from achieving stable and complete responses. Emerging evidence implicates a key role for nonmutational mechanisms including changes in cell state during early stages of acquired drug resistance. Targeting nonmutational resistance may therefore present a therapeutic opportunity to eliminate residual surviving tumor cells and impede relapse. A variety of cancer cell lines harbor quiescent, reversibly drug-tolerant âpersisterâ cells which survive cytotoxic drugs including targeted therapies and chemotherapies. These persister cells survive drug through nonmutational mechanisms which are poorly understood. Specifically targeting persister cells is a promising strategy to prevent tumor relapse. We sought to identify therapeutically exploitable vulnerabilities in persister cells using the HER2-amplified breast cancer line BT474 as an experimental model. Similar to other persister cell models, upon treatment with the HER2 inhibitor lapatinib (2uM concentration) for nine or more days, the majority of BT474 cells die, revealing a small population of quiescent surviving persister cells. Removal of lapatinib allows the persister cells to regrow and to re-acquire sensitivity to lapatinib. Subsequent lapatinib treatment re-derives persister cells. The reversibility of persister cell drug resistance indicates a nonmutational resistance mechanism. Here we provide RNAseq gene expression profiling data generated from parental BT474 cells compared to BT474 persister cells generated from nine days of treatment with 2 uM lapatinib. These data can be used to identify genes and pathways which are upregulated in persister cells, revealing potential therapeutic targets. 3 biological replicates of BT474 persister cells, two biological replicates of BT474 parental cells

2016-07-28 | E-GEOD-84896 | biostudies-arrayexpress

Expression data from A375 melanoma parental and persister cells

Project description:Expression data from A375 melanoma parental and persister cells

| PRJNA566397 | ENA