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Epigenetic basis of oncogenic-Kras mediated epithelial-cellular proliferation and plasticity [Mint-ChIP)

ABSTRACT: Epigenetic basis of oncogenic-Kras mediated epithelial-cellular proliferation and plasticity [Mint-ChIP)

PROVIDER: PRJNA791347 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17297724_1.fastq.gz	Fastqsanger.gz
	SRR17297724_2.fastq.gz	Fastqsanger.gz
	SRR17297725_1.fastq.gz	Fastqsanger.gz
	SRR17297725_2.fastq.gz	Fastqsanger.gz
	SRR17297726_1.fastq.gz	Fastqsanger.gz

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Epigenetic basis of oncogenic-Kras mediated epithelial-cellular proliferation and plasticity

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Epigenetic basis of oncogenic-Kras mediated epithelial-cellular proliferation and plasticity [Mint-ChIP)

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Transcription profiling of human lung epithelial cells ollowing oncogenic KRAS expression and TBK1 suppression or infection with oncogenic KRAS (G12V) - SuperSeries

Project description:The proto-oncogene KRAS is mutated in a wide array of human cancers, most of which are aggressive and respond poorly to standard therapies. Although the identification of specific oncogenes has led to the development of clinically effective, molecularly targeted therapies in some cases, KRAS has remained refractory to this approach. An alternative strategy for targeting KRAS is to identify gene products that, when suppressed or inhibited, result in cell death only in the presence of an oncogenic allele. Here we have used systematic RNA interference (RNAi) to detect synthetic lethal partners of oncogenic KRAS and found that the non-canonical IkB kinase, TBK1, was selectively essential in cells that harbor mutant KRAS. Suppression of TBK1 induced apoptosis specifically in human cancer cell lines that depend on oncogenic KRAS expression. In these cells, TBK1 activated NF- B anti-apoptotic signals involving cREL and BCL-XL that were essential for survival, providing mechanistic insights into this synthetic lethal interaction. These observations identify TBK1 as a potential therapeutic target in KRAS mutant tumors and establish a general approach for the rational identification of co-dependent pathways in cancer. This SuperSeries is composed of the following subset Series:; GSE17643: Profiling of immortalized human lung epithelial cells following oncogenic KRAS expression and TBK1 suppression; GSE17671: Profiling of immortalized human lung epithelial cells following infection with oncogenic KRAS (G12V) Experiment Overall Design: Refer to individual Series

2009-10-31 | E-GEOD-17672 | biostudies-arrayexpress

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Project description:We perfromed scRNA-seq on normal and Kras mutant mouse lung epithelial cells.

2021-12-22 | GSE183875 | GEO

Epigenetic basis of oncogenic-Kras mediated epithelial-cellular proliferation and plasticity [RNA-Seq]

Project description:We perfromed RNA-seq on normal and Kras mutant mouse lung epithelial cells.

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Epigenetic basis of oncogenic-Kras mediated epithelial-cellular proliferation and plasticity [ATAC-seq]

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Oncogenic KRAS Regulates Tumor Cell Signaling via Stromal Reciprocation

Project description:Oncogenic mutations in tumor cells regulate signaling both within tumor cells and heterotypic stromal cells. However, whether oncogenes regulate tumor cell signaling via stromal cells is poorly understood. Here we show that oncogenic KRAS (KRAS-G12D) uniquely regulates tumor cell signaling via stromal cells. By combining cell-specific proteome labeling with phosphoproteomic multiplexing we conducted a multivariate analysis of heterocellular KRAS-G12D signaling in Pancreatic Ductal Adenocarcinoma (PDA) cells. By engaging heterotypic fibroblasts, KRAS-G12D drives unique reciprocal signaling in tumor cells to employ additional kinases and double the number of regulated signaling nodes from cell-autonomous KRAS-G12D. Heterocellular signaling produces a distinct tumor cell phosphoproteome, total proteome, and increase mitochondria capacity via an IGF1R/AXL-AKT axis. Reciprocal KRAS-G12D phenotypes require a heterocellular context and are unreachable by cell-autonomous KRAS-G12D alone. These results demonstrate oncogene signaling should be viewed as a heterocellular process and our existing homocellular perspective underrepresents the extent of oncogene signaling in cancer.

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