Investigation of hepatocarcinogenic mechanisms by comprehensive ahalysis of cellular signaling responding to oxidative stress

2017 Fiscal Year Final Research Report

• Project/Area Number: 26293179
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Partial Multi-year Fund
• Section: 一般
• Research Field: Gastroenterology
• Research Institution: Kawasaki Medical School
• Principal Investigator: Hino Keisuke 川崎医科大学, 医学部, 教授 (80228741)
• Co-Investigator(Kenkyū-buntansha): 原 裕一 川崎医科大学, 医学部, 講師 (60550952) ; 仁科 惣治 川崎医科大学, 医学部, 講師 (70550961) ; 岸 文雄 川崎医科大学, 医学部, 教授 (40153077) ; 池田 正徳 鹿児島大学, 医歯学域医学系, 教授 (30315767)
• Project Period (FY): 2014-04-01 – 2018-03-31
• Keywords: 酸化ストレス / 活性酸素種 / 細胞内シグナル / ミトコンドリア

Outline of Final Research Achievements

We investigated the mechanisms underlying oxidative stress induces hepatocarcinogenesis in terms of cellular signaling and mitochondria quality control. Oxidative stress modified cellular signaling for glycolysis and apoptosis through activation of several kinase. These changes were cancelled by antioxidant, N-acetyl cysteine. Mitochondria is the main site of ROS production. Therefore, mitochondria quality control is critical for controlling oxidative stress. We found that iron loss reduces the development of liver tumors in NASH-rerlated hepatocarcinogenic mouse model through induction of mitochondria quality control.

Free Research Field

肝臓病学、肝発癌、酸化ストレス