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CRISPR genome-wide synthetic lethality screens of KRAS-driven mouse pancreatic ductal adenocarcinoma cells

ABSTRACT: CRISPR genome-wide synthetic lethality screens of KRAS-driven mouse pancreatic ductal adenocarcinoma cells

PROVIDER: PRJNA680493 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17065864_1.fastq.gz	Fastqsanger.gz
	SRR17065864_2.fastq.gz	Fastqsanger.gz
	SRR17065865_1.fastq.gz	Fastqsanger.gz
	SRR17065865_2.fastq.gz	Fastqsanger.gz
	SRR17065866_1.fastq.gz	Fastqsanger.gz

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CRISPR genome-wide synthetic lethality screens of KRAS-driven mouse pancreatic ductal adenocarcinoma cells

Project description:We performed CRISPR genome-wide synthetic lethality screens to identify genetic vulnerabilities and chemogenetic interactions in KRAS-driven pancreatic cancer. We identify ERAD as a genetic target that synergizes with FTS treatment and we show that FTS treatment induces ER stress, which was further enhanced by inhibition of ERAD, leading to synergistic induction of apoptosis in pancreatic tumor cells. Altogether, our screens enable us to identify combination therapies for cancer treatment.

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Project description:Many human oncogenes are challenging therapeutic targets. An alternative to direct targeting of oncogenes is to perform “synthetic lethality” screens for genes that are essential only in the context of specific cancer-causing mutations. We used high-throughput RNA interference (RNAi) to identify synthetic lethal interactions in cancer cells harboring mutant KRAS, the most commonly mutated human oncogene. We find that cells that are dependent on mutant KRAS exhibit sensitivity to suppression of the serine/threonine kinase STK33 irrespective of tissue origin, whereas STK33 is not required by KRAS-independent cells. STK33 promotes cancer cell viability in a kinase activity-dependent manner by regulating the suppression of mitochondrial apoptosis mediated through S6K1-induced inactivation of the death agonist BAD selectively in mutant KRAS-dependent cells. These observations identify STK33 as a target for treatment of the broad spectrum of mutant KRAS-driven cancers, and demonstrate the potential of RNAi screens for discovering critical functional dependencies created by oncogenic mutations that may enable therapeutic intervention for cancers associated with “undruggable” genetic alterations.

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