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Targeting novel m6A reader KHSRP impairs pancreatic ductal adenocarcinoma progression via attenuating FAK signaling

ABSTRACT: Targeting novel m6A reader KHSRP impairs pancreatic ductal adenocarcinoma progression via attenuating FAK signaling

PROVIDER: PRJNA953439 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24108400_1.fastq.gz	Fastqsanger.gz
	SRR24108400_2.fastq.gz	Fastqsanger.gz
	SRR24108401_1.fastq.gz	Fastqsanger.gz
	SRR24108401_2.fastq.gz	Fastqsanger.gz
	SRR24108402_1.fastq.gz	Fastqsanger.gz

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Targeting novel m6A reader KHSRP impairs pancreatic ductal adenocarcinoma progression via attenuating FAK signaling

Project description:We report KH-type splicing regulatory protein (KHSRP) as a novel m6A reader with oncogenic functions in pancreatic ductal adenocarcinoma (PDAC). KHSRP recognizes and stabilizes its target mRNAs (e.g., MET, ITGAV and ITGB1) in an m6A-dependent manner, therefore activating downstream FAK signaling and promoting PDAC progression. Targeting KHSRP shows promising anti-tumoral effects in vitro and in vivo, indicating that KHSRP may serve as a therapeutic target for PDAC.

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Low endothelial cell FAK expression reduces pancreatic ductal adenocarcinoma liver metastasis after gemcitabine treatment

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