| Project/Area Number |
24593007
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Multi-year Fund |
|---|
| Section | 一般 |
|---|
| Research Field |
Surgical dentistry
|
|---|
| Research Institution | Tokyo Medical University (2015)
Kyorin University (2012-2014) |
|---|
Principal Investigator |
KURAGUCHI JUN 東京医科大学, 医学部, 兼任助教 (30424576)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
CHIKAZU DAICHI 東京医科大学, 医学部, 教授 (30343122)
WATANABE MASATO 東京医科大学, 医学部, 講師 (40349460)
KAKU TOORU 日本医療大学, 保健医療学部, 教授 (60133253)
SATOMI TAKAFUMI 東京医科大学, 医学部, 准教授 (70276921)
IKEDA TETSUYA 杏林大学, 医学部, 助教 (60424107)
|
|---|
| Project Period (FY) |
2012-04-01 – 2016-03-31
|
| Project Status |
Completed (Fiscal Year 2015)
|
| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2012: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
|
|---|
| Keywords | 口腔癌 / 顎骨浸潤 / mTOR / COX-2 / ｍTOR / RANKL |
|---|
| Outline of Final Research Achievements |
The roles of mammalian target of rapamycin (mTOR) and cyclooxygenase-2 (COX-2) in bone destruction induced by oral squamous cell carcinoma (OSCC) are not well understood because of the lack of an established animal model of bone resorption by OSCC. An mTOR inhibitor might be effective in controlling bone metabolism by inhibiting the phosphorylation caused by receptor activator for nuclear factor-κB ligand (RANKL)-induced mTOR activation. Also, a COX-2 inhibitor decreases the number of osteoclasts indirectly via the RANKL signaling pathway.
We suggest that osteoclast-related cytokines play important roles in the bone invasion by OSCC cells. Our findings suggest that the new combination treatment utilizing the synergistic effects of an mTOR inhibitor and a COX-2 inhibitor against osteoclastic bone resorption in OSCC invasion.
|
