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Evaluation of Injury-induced Senescence and In Vivo Reprogramming in the Skeletal Muscle
Published on: October 26, 2017
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In vivo reprogramming drives Kras-induced cancer development
Hirofumi Shibata1,2, Shingo Komura1, Yosuke Yamada1,3
1Department of Life Science Frontiers, Center for iPS Cell Research and Application (CiRA), Kyoto University, Kyoto, 606-8507, Japan.
Nature Communications
|May 27, 2018
Summary
Transient reprogramming factor expression in pancreatic cells initiates pancreatic ductal adenocarcinoma by activating ERK signaling. This highlights the role of epigenetic regulation in cancer initiation.
Area of Science:
- Oncology
- Epigenetics
- Cellular Reprogramming
Background:
- Somatic cell reprogramming involves shutting down the differentiated cell program.
- Kras mutations are implicated in pancreatic cancer, but their precise role in initiating signaling pathways requires further investigation.
Purpose of the Study:
- To investigate the impact of in vivo cellular reprogramming on Kras-induced pancreatic cancer development.
- To elucidate the role of transient reprogramming factor expression in initiating pancreatic ductal adenocarcinoma.
Main Methods:
- Transient expression of reprogramming factors in pancreatic acinar cells of Kras mutant mice.
- Analysis of acinar cell enhancer repression and ERK signaling pathway activation.
- Assessment of pancreatic ductal adenocarcinoma formation.
- Evaluation of forced expression of acinar cell-related transcription factors.
Main Results:
- Transient reprogramming factor expression repressed acinar cell enhancers and activated ERK signaling.
- Kras and p53 mutations alone were insufficient to induce ERK signaling.
- Reprogramming factor expression in Kras mutant mice led to rapid pancreatic ductal adenocarcinoma formation.
- Forced expression of acinar cell transcription factors inhibited ERK signaling and precancerous lesion development.
Conclusions:
- Transient reprogramming factor expression can initiate pancreatic cancer by persistently activating ERK signaling.
- Dedifferentiation-associated epigenetic regulations play a critical role in pancreatic cancer initiation.
- Cellular reprogramming offers insights into cancer development mechanisms.
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