The translocation of calreticulin to cell membrane by anticancer drug and the physiological significance.

2014 Fiscal Year Final Research Report

• Project/Area Number: 24590099
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Biological pharmacy
• Research Institution: Toho University
• Principal Investigator: AZUMA Yutaro 東邦大学, 薬学部, 准教授 (80231918)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: カルレティキュリン / 小胞体ストレス / アポトーシス / 抗がん剤 / 貪食

Outline of Final Research Achievements

To clarify the transition mechanisms of calreticulin (CRT) from ER to cell surface in anti-cancer drug-treated tumor cells, the expression levels of CRT on the plasma membranes of mitoxantrone or oxaliplatin -treated human colon cancer cell line HT29 cells were estimated. It revealed that the CRT on the cell membrane exhibits increased biphasic at the protein level, and the increase of early phase was result by ER stress, ROS and activation of caspase8, the increase of late phase was concerned with apoptosis. Furthermore, mAG1-labelled CRT transfected HLF cells (HLF-ER-mAG1-CRT-KDEL cells) were prepared, and analyzed by confocal laser microscope for localizes changes of CRT. It was confirmed that mAG1-CRT were aggregated and translocated from the ER to plasma membrane, in mitoxantrone or ER stress -inducing agents thapsigargin treated HLF-ER-mAG1-CRT-KDEL cells.

Free Research Field

免疫学、細胞生物学