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In vivo reprogramming drives Kras-induced cancer development

ABSTRACT: In vivo reprogramming drives Kras-induced cancer development

PROVIDER: PRJNA393216 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5807762.fastq.gz	Fastqsanger.gz
	SRR5807763.fastq.gz	Fastqsanger.gz
	SRR5807764.fastq.gz	Fastqsanger.gz
	SRR5807765.fastq.gz	Fastqsanger.gz
	SRR5807766.fastq.gz	Fastqsanger.gz

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In vivo reprogramming drives Kras-induced cancer development [expression]

Project description:Accumulation of genetic mutations is thought to be a primary cause of cancer. However, a set of genetic mutations sufficient for cancer development remains unclear in most cancers, including pancreatic cancer. Here, we examined the effect of in vivo reprogramming on Kras-induced cancer development. We first demonstrate that Kras and p53 mutations are insufficient to induce activation of ERK signaling and cancer development in the pancreas. We next show that short transient expression of reprogramming factors (1-3 days) in pancreatic acinar cells results in repression of acinar cell enhancers and reversible loss of acinar cell properties. Notably, the transient expression of reprogramming factors in Kras mutant mice is sufficient to induce robust and persistent activation of ERK signaling in acinar cells and rapid formation of pancreatic ductal adenocarcinoma (PDAC). In contrast, forced expression of acinar cell-related transcription factors inhibits pancreatitis-induced activation of ERK signaling and development of precancerous lesions in Kras-mutated acinar cells.

2018-05-16 | GSE100840 | GEO

In vivo reprogramming drives Kras-induced cancer development [ChIP-seq]

2018-05-16 | GSE100841 | GEO

In vivo reprogramming drives Kras-induced cancer development.

Project description:The faithful shutdown of the somatic program occurs in the early stage of reprogramming. Here, we examined the effect of in vivo reprogramming on Kras-induced cancer development. We show that the transient expression of reprogramming factors (1-3 days) in pancreatic acinar cells results in the transient repression of acinar cell enhancers, which are similarly observed in pancreatitis. We next demonstrate that Kras and p53 mutations are insufficient to induce ERK signaling in the pancreas. Notably, the transient expression of reprogramming factors in Kras mutant mice is sufficient to induce the robust and persistent activation of ERK signaling in acinar cells and rapid formation of pancreatic ductal adenocarcinoma. In contrast, the forced expression of acinar cell-related transcription factors inhibits the pancreatitis-induced activation of ERK signaling and development of precancerous lesions in Kras-mutated acinar cells. These results underscore a crucial role of dedifferentiation-associated epigenetic regulations in the initiation of pancreatic cancers.

| S-EPMC5970190 | biostudies-literature

In vivo reprogramming drives Kras-induced cancer development

Project description:This SuperSeries is composed of the SubSeries listed below.

2018-05-16 | GSE100842 | GEO

In vivo reprogramming drives dedifferentiation and enhances liver regeneration

Project description:In vivo reprogramming drives dedifferentiation and enhances liver regeneration

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GNPS - Oncogenic KRAS and BRAF drive metabolic reprogramming in colorectal cancer JEH 2016

Project description:Multiplexed PRM analysis for metabolic reprogramming in isogenic cell lines with KRAS or BRAF mutations.

2016-02-01 | MSV000079486 | GNPS

Oncogenic KRAS and BRAF drive metabolic reprogramming in colorectal cancer JEH 2016

Project description:Multiplexed PRM analysis for metabolic reprogramming in isogenic cell lines with KRAS or BRAF mutations.

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DMRT1-mediated reprogramming drives development of cancer resembling human germ cell tumors with features of totipotency

Project description:In vivo reprogramming provokes a wide range of cell fate conversion. Here, we discover that in vivo induction of higher levels of OSKM in mouse somatic cells leads to increased expression of primordial germ cell (PGC)-related genes and provokes genome-wide erasure of genomic imprinting, which takes place exclusively in PGCs. Moreover, the in vivo OSKM reprogramming results in development of cancer that resembles human germ cell tumors. Like a subgroup of germ cell tumors, propagated tumor cells differentiate into trophoblasts. Moreover, these tumor cells give rise to induced pluripotent stem cells (iPSCs) with expanded differentiation potential into trophoblasts. Remarkably, the tumor-derived iPSCs are able to contribute to non-neoplastic somatic cells in adult mice. Mechanistically, DMRT1, which is expressed in PGCs, drives the reprogramming and propagation of the tumor cells in vivo. Furthermore, the DMRT1-related epigenetic landscape is associated with trophoblast competence of the reprogrammed cells and provides a therapeutic target for germ cell tumors. These results reveal an unappreciated route for somatic cell reprogramming and underscore the impact of reprogramming in development of germ cell tumors.

2021-07-20 | GSE149499 | GEO

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Project description:In vivo reprogramming drives Kras-induced cancer development [expression]

| PRJNA393220 | ENA

Aberrant enhancer reprogramming drives hepatic carcinogenesis through global transcriptional reprogramming

Project description:Aberrant enhancer reprogramming drives hepatic carcinogenesis through global transcriptional reprogramming

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