Active glucose metabolism and tumor promotion mediated by Pkm1

2016 Fiscal Year Final Research Report

• Project/Area Number: 16K14621
• Research Category: Grant-in-Aid for Challenging Exploratory Research
• Allocation Type: Multi-year Fund
• Research Field: Tumor biology
• Research Institution: Miyagi Prefectural Hospital Organization Miyagi Cancer Center
• Principal Investigator: TANUMA Nobuhiro 地方独立行政法人宮城県立病院機構宮城県立がんセンター(研究所), がん薬物療法研究部, 主任研究員 (40333645)
• Project Period (FY): 2016-04-01 – 2017-03-31
• Keywords: Pkm / グルコース代謝 / オートファジー

Outline of Final Research Achievements

In this study, we explored how Pkm1 promotes tumor growth/survival. We found that the mode of Pkm1's action is tumor cell-intrinsic. Pkm1-expressing cells combine active TCA cycle and lower ROS levels in mitochondria through mitophagy. Importantly, this metabolic rewiring by Pkm1 impedes neither pentose phosphate pathway nor purine synthesis. Our results unveil tumor-promoting function of Pkm1.

Free Research Field

腫瘍学