2012 Fiscal Year Final Research Report
Mechanisms of oncogenic stress evolution caused by obesity
| Project/Area Number |
23701040
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Carcinogenesis
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| Research Institution | National Center for Geriatrics and Gerontology |
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Principal Investigator |
YAMAKOSHI Kimi 独立行政法人国立長寿医療研究センター, 老化機構研究部, 室長 (50423398)
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| Project Period (FY) |
2011 – 2012
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| Keywords | 肥満 / 発癌ストレス / 癌抑制遺伝子 / p16^<INK4a> / p53 |
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| Research Abstract |
Using a bioluminescence imaging system for p16^<INK4a> expression in living mice, we show that oncogenic insults such as obesity and p53 inactivation provoke de-repression of p16INK4a expression in progenitors of adipose tissue. p53 inactivation increases DNA damage and reactive oxygen species(ROS) in progenitors of adipose tissues, indicating that obesity generates oncogenic stress in these cells.
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[Journal Article] DNA damage signaling triggers degradation of histone methyltransferases through APC/CCdh1 in senescent cells.2012
Author(s)
Takahashi, A., Imai, Y., Yamakoshi, K., Kuninaka, S., Ohtani, N., Yoshimoto, S., Hori, S., Tachibana, M., Anderton, E., Takeuchi, T., Shinkai, Y., Peters, G., Saya, H., Hara, E.
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Journal Title
Molecular Cell
Volume: 45(1)
Pages: 123-131
Peer Reviewed
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