Resolution of cancer metastasis mechanism by decrease of cell adhesion and identification of controlled drug

• Project/Area Number: 26861703
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Surgical dentistry
• Research Institution: Chiba University
• Principal Investigator: HIGO Morihiro 千葉大学, 医学部附属病院, 助教 (60724383)
• Project Period (FY): 2014-04-01 – 2016-03-31
• Project Status: Completed (Fiscal Year 2015)
• Budget Amount: ¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000); Fiscal Year 2015: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000); Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
• Keywords: 発がん / がん遺伝子 / 浸潤・転移 / KLK13 / 口腔扁平上皮癌

Outline of Final Research Achievements

Various studies were reported that the important issues were the regulation of cancer metastasis, anticancer drug resistance, and radiation resistance. We identified the gene of Kallikrein-related peptidase 13(KLK13) that promoted the expression of cadherin complex and desmosome component. In this study, we confirmed the enhanced expression of these elements and the depression effect of metastatic ability in vivo by a drug enhancing KLK13 action. Therefore, these results are very useful to develop a cancer metastasis inhibitor.