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Status |
Public on May 16, 2018 |
Title |
In vivo reprogramming drives Kras-induced cancer development [ChIP-seq] |
Organism |
Mus musculus |
Experiment type |
Genome binding/occupancy profiling by high throughput sequencing
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Summary |
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.
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Overall design |
Analyzing H3K27ac in promoter and enhancer of the pancreas of with or without OSKM induction/ Caerulein treatment
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Contributor(s) |
Shibata H, Ukai T, Yamamoto T, Yamada Y |
Citation(s) |
29802314 |
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Submission date |
Jul 05, 2017 |
Last update date |
Jul 25, 2021 |
Contact name |
Yasuhiro Yamada |
E-mail(s) |
yyamada@m.u-tokyo.ac.jp
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Organization name |
University of Tokyo
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Department |
Department of Molecular Pathology
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Street address |
7-3-1 Hongo, Bunkyo-ku
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City |
Tokyo |
ZIP/Postal code |
113-0033 |
Country |
Japan |
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Platforms (1) |
GPL19057 |
Illumina NextSeq 500 (Mus musculus) |
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Samples (14)
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This SubSeries is part of SuperSeries: |
GSE100842 |
In vivo reprogramming drives Kras-induced cancer development |
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Relations |
BioProject |
PRJNA393221 |
SRA |
SRP111152 |