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ACGH and high-throughput transcriptome profiling of non-small cell lung cancer cell lines sensitive or resistant to CPL304110 FGFR inhibitor

ABSTRACT: aCGH and high-throughput transcriptome profiling of non-small cell lung cancer cell lines sensitive or resistant to CPL304110 FGFR inhibitor

PROVIDER: PRJNA782314 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16993316_1.fastq.gz	Fastqsanger.gz
	SRR16993316_2.fastq.gz	Fastqsanger.gz
	SRR16993317_1.fastq.gz	Fastqsanger.gz
	SRR16993317_2.fastq.gz	Fastqsanger.gz
	SRR16993318_1.fastq.gz	Fastqsanger.gz

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aCGH profiling for non-small cell lung cancer cell lines sensitive or resistant to CPL304110 FGFR inhibitor

Project description:aCGH profiling for non-small cell lung cancer cell lines sensitive or resistant to CPL304110 FGFR inhibitor

| PRJNA782316 | ENA

aCGH profiling for non-small cell lung cancer cell lines sensitive or resistant to CPL304110 FGFR inhibitor

Project description:FGFR signalling is one of the most prominent pathways involved in cell growth and development, as well as cancer progression. FGFR1 amplification occurs in approximately 20% of all squamous cell lung carcinomas (SCC) - one of the most common subtypes of non-small cell lung carcinoma (NSCLC), indicating FGFR as a potential target for the new anti-cancer therapies. However, acquired resistance to this type of therapies remains a clinical issue. Here, we investigated the NSCLC cell lines response and potential mechanism of acquired resistance to novel selective FGFR inhibitor CPL304110. We found that despite significant genomic differences between CPL304110-sensitive cell lines, their resistant variants were characterized by upregulated p38 expression/phosphorylation, as well as enhanced expression of genes involved in MAPK signalling. We revealed that p38 inhibition restored sensitivity to CPL304110 in these cells. Moreover, overexpression of this kinase in parental cells led to impaired response to FGFR inhibition, thus confirming that p38 MAPK is a driver of resistance to a novel FGFR inhibitor. Taken together, our results provide an insight into the potential direction for NSCLC targeted therapy.

2021-11-23 | GSE189268 | GEO

In vitro expression in FGFR inhibitor sensitive and resistant cell lines

Project description:The challenge of developing effective pharmacodynamic biomarkers for pre-clinical and clinical testing of FGFR signalling inhibition is significant. Assays that rely on the measurement of phospho-protein epitopes can be limited by the availability of effective antibody detection reagents. Transcript profiling enables accurate quantification of many biomarkers and a broader representation of pathway modulation. To identify dynamic transcript biomarkers of FGFR signalling inhibition by AZD4547, a potent inhibitor of FGF receptor 1, 2 and 3, a gene expression profiling study was performed in FGFR2 amplified drug sensitive tumour cell lines.

2016-08-25 | E-MTAB-4749 | biostudies-arrayexpress

High-throughput transcriptome profiling of non-small cell lung cancer cell lines sensitive or resistant to CPL304110 FGFR inhibitor

2021-11-23 | GSE189269 | GEO

High-throughput transcriptome profiling of non-small cell lung cancer cell lines sensitive or resistant to CPL304110 FGFR inhibitor

Project description:High-throughput transcriptome profiling of non-small cell lung cancer cell lines sensitive or resistant to CPL304110 FGFR inhibitor

| PRJNA782315 | ENA

aCGH and high-throughput transcriptome profiling of non-small cell lung cancer cell lines sensitive or resistant to CPL304110 FGFR inhibitor

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

2021-11-23 | GSE189270 | GEO

Integrative analysis of Multi-omics data of FGFR inhibitor

Project description:Dissection of the mechanism of action of FGFR inhibitor by multi-omic analysis

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Project description:Extended Primate aCGH

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FGFR signature

Project description:Drugs that target specific gene alterations have proven beneficial in the treatment of cancer. Because cancer cells have multiple resistance mechanisms, it is important to understand the downstream pathways of the target genes and monitor the pharmacodynamic markers associated with therapeutic efficacy. We performed a transcriptome analysis to characterize the response of various cancer cell lines. We performed a transcriptome analysis to characterize the response of various cancer cell lines to a selective fibroblast growth factor receptor (FGFR) inhibitor (CH5183284/Debio 1347), a mitogen-activated protein kinase kinase (MEK) inhibitor, or a phosphoinositide 3-kinase (PI3K) inhibitor. We treated compounds for 24 hours and purified total RNA.

2016-01-06 | E-GEOD-73024 | biostudies-arrayexpress

Gene expression profile of 31 RAS/RAF-wild-type colorectal cancer (CRC) stem-cell (SC) spheroids and 7 FGFR-inhibitor resistant CSC-SC spheroids

Project description:This study investigated mechanisms of acquired resistance to FGFR inhibitor therapy in RAS/RAF–wild-type colorectal cancer (CRC). RNA sequencing (RNA-seq) data from 47 RAS/RAF-wild-type colorectal cancer stem-cell (CRC-SC) spheroid lines previously deposited under GSE205787 were integrated with newly generated RNA-seq data from 31 additional RAS/RAF-wild-type CRC-SC spheroid lines and seven FGFR inhibitor-resistant CRC-SC derivatives. The resistant derivatives were established from parental CRC-SC spheroid lines by continuous exposure to erdafitinib or futibatinib. Comparative transcriptomic analysis between matched parental and resistant lines revealed consistent upregulation of EGFR and downregulation of PTPROt, a truncated isoform of PTPRO, in resistant derivatives. Gene set enrichment analysis further indicated activation of EGFR-related signaling pathways in FGFR inhibitor-resistant spheroids. In addition, the integrated RNA-seq dataset comprising 78 RAS/RAF-wild-type CRC-SC lines was used to validate the inverse correlation between EGFR and PTPRO mRNA expression, supporting the involvement of PTPROt downregulation and EGFR pathway activation in acquired resistance to FGFR inhibition.

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