Functional characterization of ESRP1 and 2 in HNSCC.
| Project/Area Number |
24791764
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Otorhinolaryngology
|
|---|
| Research Institution | University of Yamanashi |
|---|
Principal Investigator |
ISHII Hiroki 山梨大学, 総合研究部, 助教 (40568250)
|
|---|
| Project Period (FY) |
2012-04-01 – 2015-03-31
|
| Project Status |
Completed (Fiscal Year 2014)
|
| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2014: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2013: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2012: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
|
|---|
| Keywords | ESRP1/2 / EMT / RNA splicing / Rac1b / dEF1/SIP1 / ESRP1 / ESRP2 / 頭頸部癌 / 選択的RNAスプライシング / EMT関連転写因子 / CD44 |
|---|
| Outline of Final Research Achievements |
ESRP1 (epithelial splicing regulatory protein 1) and ESRP2 regulate alternative splicing events associated with EMT, and these proteins are down-regulated during EMT. We examined that expression of both ESRP1 and ESRP2 is plastic. During HNSCC carcinogenesis,both are up-regulated relative to their levels in normal epithelium but down-regulated in invasive fronts into stroma. In HNSCC cell lines, ESRP1 and ESRP2 suppress cell motility of HNSCC via distinct mechanisms: knockdown of ESRP1 affects the dynamics of the actin cytoskeleton via inducing Rac1b, whereas knockdown of ESRP2 represses cell-cell adhesion through increased expression of EMT-associated transcription factors. Down-regulation of ESRP1 and ESRP2 is thus closely associated with a motile phenotype of cancer cells
|
Report
(4 results)
Research Products
(6 results)
