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Identification of transcriptional difference between Imatinib-sensitive and resistant patients with gastrointerstinal stromal tumor (GIST)

ABSTRACT: Identification of transcriptional difference between Imatinib-sensitive and resistant patients with gastrointerstinal stromal tumor (GIST)

PROVIDER: PRJNA655677 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12401400_1.fastq.gz	Fastqsanger.gz
	SRR12401400_2.fastq.gz	Fastqsanger.gz
	SRR12401401_1.fastq.gz	Fastqsanger.gz
	SRR12401401_2.fastq.gz	Fastqsanger.gz
	SRR12401402_1.fastq.gz	Fastqsanger.gz

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Identification of transcriptional difference between Imatinib-sensitive and resistant patients with gastrointerstinal stromal tumor (GIST)

Project description:Purpose: The goals of this study are to characterize the transcriptional dysregulation of GIST. More importantly, the transcriptome differences betweeen Imatinib-sensitive and resistant patients are compared to identify RNAs that may impact Imatinib resistance. Methods: High-throughput RNA sequencing (RNA-seq) was employed to capture the transcriptional changes in GIST compared to normal samples. RSEM was used to quantify gene expression and DESeq2 was utilized to compared expression changes between different sample groups.

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Project description:Acquired resistance of gastrointestinal stromal tumors (GISTs) to imatinib mesylate (IM) is one of the most critical challenges in GIST therapy. Here we show that a long-term culture of GIST T-1 cells with IM induces clonal heterogeneity resulting in the appearance of cancer cells exhibiting activation of the FGFR-signaling pathway which was associated with KIT loss. The first one was due to the overexpression of FGFR1/2 and increased production of FGF-2 ligand. These events maintained GIST resistance to IM and rendered these GIST cells highly sensitive to all types of pan-FGFR-inhibitors used in the current study. Knockout of FGFR2 in this GIST subclone significantly attenuated pro-apoptotic and anti-proliferative activities of infigratinib (BGJ 398) both in vitro and in vivo, thereby suggesting the activation of FGFR-signaling pathway via FGFR2-mediated axis as the predominant molecular mechanism in these GIST cells. Collectively, the extended inhibition of KIT-signaling in GISTs induces clonal heterogeneity of cancer cells and might change the tumor’s sensitivity to FGFR-inhibitors due to selection of cancer cells with an FGFR-overactivated pathway.

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