| Project/Area Number |
25640060
|
|---|
| Research Category |
Grant-in-Aid for Challenging Exploratory Research
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Tumor biology
|
|---|
| Research Institution | Tokyo Medical and Dental University |
|---|
Principal Investigator |
Ito Hiromitsu 東京医科歯科大学, 医歯(薬)学総合研究科, 助教 (80645474)
|
|---|
| Project Period (FY) |
2013-04-01 – 2016-03-31
|
| Project Status |
Completed (Fiscal Year 2015)
|
| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2014: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
Fiscal Year 2013: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
|
|---|
| Keywords | 癌幹細胞 / 浸潤・転移 / エピゲノム / 膵臓癌 / 転移 / DCLK-1 |
|---|
| Outline of Final Research Achievements |
Patients with pancreatic cancer typically develop tumor invasion and metastasis in the early stage. We previously examined the proteasome activity of CSCs and constructed a real-time visualization system for human pancreatic CSCs. In the present study, we found that CSCs were highly metastatic and dominantly localized at the invading tumor margins in a liver metastasis model. Microarray and siRNA screening assays showed that DCLK1 was predominantly expressed with histone modification in pancreatic CSCs with invasive and metastatic potential. Overexpression of DCLK1 led to amoeboid morphology, which promotes the migration of pancreatic cancer cells. Knockdown of DCLK1 profoundly suppressed in vivo liver metastasis of pancreatic CSCs. With clinical samples, our studies revealed that DCLK1 may be a promising epigenetic and therapeutic target in human pancreatic cancer.
|
