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TGFbeta treatment drives iKPC PDAC cells to bypass KRAS* dependency

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

PROVIDER: PRJNA627427 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11589383_1.fastq.gz	Fastqsanger.gz
	SRR11589383_2.fastq.gz	Fastqsanger.gz
	SRR11589384_1.fastq.gz	Fastqsanger.gz
	SRR11589384_2.fastq.gz	Fastqsanger.gz
	SRR11589385_1.fastq.gz	Fastqsanger.gz

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TGFbeta treatment drives iKPC PDAC cells to bypass KRAS* dependency

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.

2020-04-27 | GSE149130 | GEO

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.

2020-04-27 | GSE149126 | GEO

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:USP21 promotes PDAC tumor cells to bypass KRAS* dependency. To dissect the molecular mechanism, we conducted RNA-seq analysis comparing iKPC cancer cells overexpressing GFP, wildtype USP21 and enzyme-dead USP21 at day 3 after KRAS* extinction. KRAS*-expressing iKPC cells with GFP overexpression are positive control.

2021-09-17 | GSE178860 | GEO

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.

2020-04-27 | GSE149129 | GEO

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).

2019-09-04 | GSE134686 | GEO

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

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

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RNAseq data comparing HDAC5 eccaper PDAC cells with HDAC5 knockdown and scramble control

Project description:HDAC5 drives PDAC cells to bypass KRAS* dependency. To dissect the molecular mechanisms that regulated by overexpressed HDAC5 in escaper cells, we conducted RNA-seq analysis of HDAC5 escaper PDAC cells knocking down of HDAC5 or scramble shRNA control.

2020-04-27 | GSE149127 | GEO

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

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

| PRJNA627428 | ENA

Identification of genes regulated by NFAT5-SMADs complex

Project description:Oncogenic KRAS is now considered a druggable target; however, multiple mechanisms contribute to the development of resistance to KRAS-targeted therapy. A significant factor in therapy resistance is the alteration in cell state or cellular plasticity, exemplified by the epithelial-to-mesenchymal transition (EMT) phenotype. In pancreatic ductal adenocarcinoma (PDAC), the negative correlation between addiction to oncogenic KRAS signaling and EMT has been observed, yet the role of cell plasticity and its underlying mechanisms in governing resistance remain unclear. Our findings reveal that the pivotal EMT driver, TGFβ, facilitates KRAS bypass in PDAC through the nuclear factor NFAT5. NFAT5 interacts with canonical TGFβ factors SMAD3 and SMAD4, inducing EMT and therapy resistance. To unravel the regulatory role of the NFAT5-SMADs complex in KRAS* bypass, we conducted transcriptomic analysis in TGFβ-treated, KRAS*-depleted iKPC spheroids.

2024-10-09 | GSE252836 | GEO

Stromal-derived NRG1 enables oncogenic KRAS bypass in pancreas cancer

Project description:Activating KRAS mutations (KRAS*) in pancreatic ductal adenocarcinoma (PDAC) drive anabolic metabolism and support tumor maintenance. KRAS* inhibitors show initial anti-tumor activity followed by recurrence due to cancer cell intrinsic and immune mediated paracrine mechanisms. Here, we explored the potential role of cancer associated fibroblasts (CAFs) in enabling KRAS* bypass and identified CAF-derived NRG1 activation of cancer cell ERBB2/ERBB3 receptor tyrosine kinases as a mechanism by which KRAS* independent growth is supported. Genetic extinction or pharmacological inhibition of KRAS* resulted in upregulation of ERBB2 and ERBB3 expression in human and murine models, which prompted cancer cell utilization of CAF-derived NRG1 as a survival factor. Genetic depletion or pharmacological inhibition of ERBB2/ERBB3 or NRG1 abolished KRAS* bypass and synergized with KRASG12D inhibitor in combination treatments in mouse and human PDAC models. Thus, we found that CAFs can contribute to KRAS* inhibitor therapy resistance via paracrine mechanisms, providing an actionable therapeutic strategy to improve the effectiveness of KRAS* inhibitors in PDAC patients.

2023-09-22 | GSE240232 | GEO

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