Novel functions and relevance to the diseases of intracellular phospholipase A1

2017 Fiscal Year Final Research Report

• Project/Area Number: 15K07946
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Biological pharmacy
• Research Institution: Teikyo University
• Principal Investigator: Yamashita Atsushi 帝京大学, 薬学部, 教授 (80230415)
• Co-Investigator(Renkei-kenkyūsha): SASAKI YOKO (NEMOTO YOKO) 帝京大学, 薬学部, 講師 (90324110) ; HAYASHI YASUHIRO 帝京大学, 薬学部, 助教 (70582857) ; MATSUMOTO NAOKI 帝京大学, 薬学部, 助教 (40447834)
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: ホスホリパーゼA / 細胞増 / 細胞周期 / 細胞の生存 / アポトーシス / ミトコンドリア / リゾリン脂質 / リン脂質

Outline of Final Research Achievements

In the present study, we investigated the effects of DDHD1/ PA-PLA1 on the proliferation and survival of pancreatic cancer cells. DDHD1/ PA-PLA1 and its non-catalytic mutant (S537A) were expressed in the pancreatic cancer cells by the recombinant retrovirus system. The expression of DDHD1/ PA-PLA1 and S537A mutant significantly reduced the proliferation of PANC-1 cells with normal growth medium. The cell cycle analysis revealed that the expression of DDHD1/ PA-PLA1 and S537A mutant significantly decreased the G0/G1 cells and increased G2/M cells, suggesting that the expression caused the G2/M cell cycle arrest. The expression of DDHD1/ PA-PLA1 and S537A mutant significantly increased the mitochondrial respiration and membrane potential. Our results suggest that DDHD1/ PA-PLA1 is involved in the regulation of G2/M cell cycle transition and mitochondrial function and the dysregulation of DDHD1/ PA-PLA may be lead to the reduced cell proliferation of pancreatic cancer cells.

Free Research Field

生化学、脂質生物学、分子生物学、細胞生物学