Studies in experimental animals of oral cancer metastasis suppression using a nutritional immunity (EPA)

2015 Fiscal Year Final Research Report

• Project/Area Number: 25463114
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Surgical dentistry
• Research Institution: Kumamoto University
• Principal Investigator: Ogi Hidenao 熊本大学, 大学院生命科学研究部(医), 助教 (10315426)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: 口腔がん / 転移 / EPA / TNF-α / TNFR1

Outline of Final Research Achievements

Cancer cells (GSAS/N5) increased invasive activity 7-fold in a TNF-α receptor TNFR1-dependent manner and enhanced TNF- α and TNFR1 mRNA expression. In the highly metastatic cells, NF-B activation was up-regulated via elevated phosphorylation of Akt and Ikk/ in the signaling pathway and secretion of TNF-α ,active MMP-2 and MMP-9 increased.; TNF- activates NF-κB and activated NF-κB induces further TNF- secretion, leading to increase of active MMP release and promotion of invasion and metastasis of the cells. GSAS/N5 cells that were injected into the nude mouse tongue and harvested from metastasized lungs multiplied angiopoietin-like 4 (angptl4) expression with enhanced migration activity, which indicated a possible involvement of angptl4 in lung metastasis of the cells. These results suggest that TNF-α and angptl4 promote metastasis of the oral cancer cells, thus these molecules may be therapeutic targets for patients with tongue cancer.

Free Research Field

歯科口腔外科