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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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Protein-RNA interaction dynamics downstream of KRAS activation reveals key regulators of oncogenic KRAS driven cancers.

Project description:Oncogenic KRAS mutations rewires cellular signaling, leading to significant alterations in gene expression. RNA-binding proteins (RBPs) play a pivotal role in gene expression regulation by post-transcriptionally controlling various aspects of RNA metabolism. It becomes clear that interactions between RBPs and RNA are frequently dysregulated in numerous cancers. However, how the oncogenic KRAS mutations reshape the post-transcriptional regulatory network mediated by RBPs remain poorly understood. In this study, we have systematically dissected oncogenic KRAS driven alternation of RNA-RBP networks. We identified several cancer-associated RBPs with either increased or decreased RNA binding upon oncogenic KRAS, including PDCD11, which is essential for the viability of KRAS mutant cancers, and ELAVL2, which regulates SNAIL and affects cell migration in KRAS mutant lung cancers. Our study serves as a crucial resource for elucidating RBP regulatory networks in KRAS mutant cancers and may provide new avenues for therapeutic strategies targeting KRAS mutant malignancies.

2025-05-07 | PXD053310 | Pride

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