Dose T Cell Death-Associated Gene 8 (TDAG8), One of Proton-Sensing G-protein-coupled Receptors, Play A Roll in 3-Methylcholanthrene-induced Tumor Formation?

2015 Fiscal Year Final Research Report

• Project/Area Number: 26640087
• Research Category: Grant-in-Aid for Challenging Exploratory Research
• Allocation Type: Multi-year Fund
• Research Field: Tumor biology
• Research Institution: Gunma Institute of Public Health and Environmental Sciences
• Principal Investigator: Murata Naoya 群馬県衛生環境研究所, その他部局等, 研究企画係研究員 (00533473)
• Co-Investigator(Renkei-kenkyūsha): OKAJIMA Fumikazu 群馬大学, 生体調節研究所, 教授 (30142748)
• Project Period (FY): 2014-04-01 – 2016-03-31
• Keywords: 発癌 / pH感知性受容体 / TDAG8

Outline of Final Research Achievements

We analyzed a role of the host immunity in the tumor formation using TDAG8-receptor-deficiency mice. As a result, the tumor formation was induced with a single subcutaneous dosage of chemical carcinogen 3-methylcholanthrene(3-MCA) in more than 90% of the wild type, but was reduced to its half in the TDAG8-deficiency type. However, immunohistological examination show no significant difference in the degree of immune cells( e.g. CD3-positive T cell)infiltration to the tumor tissues between both types. In addition, no significant difference was found between both types not only in the tumor formation with inoculation of 3-MCA-induced mouse fibrosarcoma cell strain (MC57G) but also in MC57G-induced cytotoxic activity. Thus, it was supposed that the suppressive effect on the tumor formation found in TDAG8-deficiency type is induced by indirect cellular or humoral regulation mechanisms of the host immunity, but not by direct cytotoxic activity by the immune cells, such as T cells.

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