| Project/Area Number |
22659177
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Single-year Grants |
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| Research Field |
Endocrinology
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| Research Institution | Chiba University |
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Principal Investigator |
TANAKA Tomoaki 千葉大学, 大学院・医学研究院, 講師 (50447299)
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| Co-Investigator(Kenkyū-buntansha) |
龍野 一郎 東邦大学, 医療センター佐倉病院, 教授 (80282490)
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| Project Period (FY) |
2010 – 2011
|
| Project Status |
Completed (Fiscal Year 2011)
|
| Budget Amount *help |
¥3,210,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥210,000)
Fiscal Year 2011: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2010: ¥2,300,000 (Direct Cost: ¥2,300,000)
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| Keywords | p53 / 転写因子 / エネルギー調節 / 細胞内代謝 / エピジェネティクス |
|---|
| Research Abstract |
Recent epidemiologic evidence suggests that type 2 diabetes and obesity are at significantly higher risk for many types of cancer. In this context, p53 has been shown to control mitochondrial functions through regulation of ROS and cell metabolism, implicating its potential role in biologic links between diabetes and cancer. Here we have explored p53 targets to regulate cell metabolism using ChIP- and RNA-sequencing and identified GLS2, a key enzyme to convert glutamine to glutamate, thereby a regulator of glutathione synthesis and ATP production via TCA cycle. GLS2 overexpression inhibited cancer cell growth as well as invasion in both vitro and vivo, suggesting its potential role for tumor suppression. Thus, p53-GLS2 pathway may contribute to the common pathogenesis between life-style related diseases and cancer.
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