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Obesity Suppresses Cell-Competition-Mediated Apical Elimination of RasV12-Transformed Cells from Epithelial Tissues

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Please use this identifier to cite or link to this item:http://hdl.handle.net/2115/70992

Title: Obesity Suppresses Cell-Competition-Mediated Apical Elimination of RasV12-Transformed Cells from Epithelial Tissues
Authors: Sasaki, Ayana Browse this author
Nagatake, Takahiro Browse this author
Egami, Riku Browse this author
Gu, Guoqiang Browse this author
Takigawa, Ichigaku Browse this author →KAKEN DB
Ikeda, Wataru Browse this author
Nakatani, Tomoya Browse this author
Kunisawa, Jun Browse this author
Fujita, Yasuyuki Browse this author →KAKEN DB
Issue Date: 24-Apr-2018
Publisher: Cell Press
Journal Title: Cell Reports
Volume: 23
Issue: 4
Start Page: 974
End Page: 982
Publisher DOI: 10.1016/j.celrep.2018.03.104
Abstract: Recent studies have revealed that newly emerging transformed cells are often eliminated from epithelial tissues via cell competition with the surrounding normal epithelial cells. This cancer preventive phenomenon is termed epithelial defense against cancer (EDAC). However, it remains largely unknown whether and how EDAC is diminished during carcino-genesis. In this study, using a cell competition mouse model, we show that high-fat diet (HFD) feeding substantially attenuates the frequency of apical elimination of RasV12-transformed cells from intestinal and pancreatic epithelia. This process involves both lipid metabolism and chronic inflammation. Furthermore, aspirin treatment significantly facilitates eradication of transformed cells from the epithelial tissues in HFD-fed mice. Thus, our work demonstrates that obesity can profoundly influence competitive interaction between normal and transformed cells, providing insights into cell competition and cancer preventive medicine.
Rights: http://creativecommons.org/licenses/by-nc-nd/4.0/
Type: article
URI: http://hdl.handle.net/2115/70992
Appears in Collections:遺伝子病制御研究所 (Institute for Genetic Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 藤田 恭之

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