Dissecting the roles of metabolism in the development of cancer by means of the mitochondrial hyperactive model mice

2015 Fiscal Year Final Research Report

• Project/Area Number: 26640082
• Research Category: Grant-in-Aid for Challenging Exploratory Research
• Allocation Type: Multi-year Fund
• Research Field: Tumor biology
• Research Institution: Nagasaki University
• Principal Investigator: YAMAMOTO Kazuo 長崎大学, 医歯薬学総合研究科(医学系), 准教授 (70255123)
• Project Period (FY): 2014-04-01 – 2016-03-31
• Keywords: ミトコンドリア / トランスジェニックマウス / 白血病 / リンパ腫 / 代謝

Outline of Final Research Achievements

To investigate the roles of metabolism in cancer development, leukemia model mice and mitochondrial hyperactive transgenic mice were analyzed. Mitochondrial hyperactivation resulted in significant extension of the death caused by leukemia. The key protein responsible for this phenomenon was turned out to localize as dots in cytoplasm any other than mitochondria, the Golgi body, endoplasmic reticulum, peroxisome, nor endosome. Transcriptome analysis revealed that a few specific transcription factors governed the unique transcription profile in the cells overexpressing this protein. As the protein synthesis was upregulated in these cells, the effect induced by this protein was analyzed in vivo. The result suggested that the rate of protein synthesis was raised by mitochondrial hyperactivation.

Free Research Field

分子細胞生物学