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RNAseq data comparing iKPC PDAC tumors with KRAS* expression (ON) and KRAS extinction (OFF)

ABSTRACT: RNAseq data comparing iKPC PDAC tumors with KRAS* expression (ON) and KRAS extinction (OFF)

PROVIDER: PRJNA627428 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11589375_1.fastq.gz	Fastqsanger.gz
	SRR11589375_2.fastq.gz	Fastqsanger.gz
	SRR11589376_1.fastq.gz	Fastqsanger.gz
	SRR11589376_2.fastq.gz	Fastqsanger.gz
	SRR11589377_1.fastq.gz	Fastqsanger.gz

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RNAseq data comparing iKPC PDAC tumors with KRAS* expression (ON) and KRAS extinction (OFF)

Project description:KRAS* is required for PDAC tumor mantainence. To dissect the molecular mechanisms that regulated by KRAS* in PDAC tumors, we conducted RNA-seq analysis of KRAS*-expressing iKPC PDAC tumors and iKPC tumors after KRAS* extinction for 24 hours.

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RNAseq data comparing GFP, wildtype USP21 and enzyme-dead USP21 overexpressing iKPC PDAC cells with KRAS* expression (on dox) and KRAS* extinction (off dox)

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RNAseq data comparing KRAS*-independent HDAC5 eccaper PDAC cells and KRAS*-dependent iKPC PDAC cells

Project description:HDAC5 drives PDAC cells to bypass KRAS* dependency. To dissect the molecular mechanisms that regulated by overexpressed HDAC5 in the bypass of KRAS* dependency, we conducted RNA-seq analysis of HDAC5 escaper PDAC cells and KRAS*-expressing iKPC PDAC cells.

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RNAseq data comparing KRAS*-independent HDAC5 eccaper PDAC cells and KRAS*-dependent iKPC PDAC cells

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Project description:TGFbeta promotes the bypass of KRAS* dependency in PDAC. To dissect the molecular mechanisms that regulated by TGFbeta in PDAC cells, we conducted RNA-seq analysis of iKPC PDAC cells with or without TGFbeta treatment.

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RNAseq data comparing GFP, wildtype USP21 and enzyme-dead USP21 overexpressing iKPC PDAC cells with KRAS* expression (on dox) and KRAS* extinction (off dox)

Project description:RNAseq data comparing GFP, wildtype USP21 and enzyme-dead USP21 overexpressing iKPC PDAC cells with KRAS* expression (on dox) and KRAS* extinction (off dox)

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TGFbeta treatment drives iKPC PDAC cells to bypass KRAS* dependency

Project description:TGFbeta treatment drives iKPC PDAC cells to bypass KRAS* dependency

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RNAseq data comparing iKPC cells overexpressing WT-USP21 and ED-USP21

Project description:USP21 belongs to ubiquitin specific protease (USP) family. To dissect the molecular mechanisms that regulated by USP21 overexpression in PDAC cells, we conducted RNA-seq analysis of iKPC PDAC cells overexpressing wild-type USP21 (WT-USP21) and enzyme dead USP21 (ED-USP21).

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Differentially expressed genes in iKRAS tumor treated with Trametinib or Kras extinction

Project description:To identify the differentially expressed gene in ikras tumors treated with Trametinib or Kras extinction.

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Determining the KRAS-regulated kinome in PDAC

Project description:Oncogenic KRAS drives cancer growth by activating diverse signaling networks, not all of which have been fully delineated. We set out to establish a system-wide profile of the KRAS-regulated kinase signaling network (kinome) in KRAS-mutant pancreatic ductal adenocarcinoma (PDAC). We knocked down KRAS expression in a panel of six cell lines, and then applied Multiplexed Inhibitor Bead/Mass Spectrometry (MIB/MS) chemical proteomics to monitor changes in kinase activity and/or expression. We hypothesized that depletion of KRAS would result in downregulation of kinases required for KRAS-mediated transforming activities, and in upregulation of other kinases that could potentially compensate for the deleterious consequences of the loss of KRAS. We identified 15 upregulated and 13 downregulated kinases in common across the panel. In agreement with our hypothesis, all 15 of the upregulated kinases have established roles as cancer drivers (e.g., SRC, TGFBR1, ILK), and pharmacologic inhibition of the upregulated kinase, DDR1, suppressed PDAC growth. Interestingly, 11 of the 13 downregulated kinases have established driver roles in cell cycle progression, particularly in mitosis (e.g., WEE1, Aurora A, PLK1). Consistent with a crucial role for the downregulated kinases in promoting KRAS-driven proliferation, we found that pharmacologic inhibition of WEE1 also suppressed PDAC growth. The unexpected paradoxical activation of ERK upon WEE1 inhibition led us to inhibit both WEE1 and ERK concurrently, which caused further potent growth suppression and enhanced apoptotic death than WEE1 inhibition alone. We conclude that system-wide delineation of the KRAS-regulated kinome can identify potential therapeutic targets for KRAS-mutant pancreatic cancer.

2022-02-17 | PXD025819 | Pride

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