| Project/Area Number |
17591483
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Thoracic surgery
|
|---|
| Research Institution | National Institute for Longevity Sciences, National Center for Geriatrics and Gerontology (2006)
Kyoto Prefectural University of Medicine (2005) |
|---|
Principal Investigator |
UEKAWA Natsuko (2006) National Institute for Longevity Sciences, National Center for Geriatrics and Gerontology, Department of Mechanism of Aging, Research fellow, (研究所)・老化機構研究部, 外来研究員 (00399594)
西村 元宏 (2005) 京都府立医科大学, 医学研究科, 助手 (00398372)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
SHIMADA Jun-ichi Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Department of Cardiovascular and Thoracic Surgery, Assistant professor, 医学研究科, 講師 (60315942)
YAOI Takeshi Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Department of Pathology and Applied Neurobiology, Research associate, 医学研究科, 助手 (40311914)
MARUYAMA Mitsuo National Institute for Longevity Sciences, National Center for Geriatrics and Gerontology, Department of Mechanism of Aging, Department head, (研究所)・老化機構研究部, 部長 (00212225)
上川 奈都子 国立長寿医療センター, 研究所・老化機構研究部, 研究員 (00399594)
|
|---|
| Project Period (FY) |
2005 – 2006
|
| Project Status |
Completed (Fiscal Year 2006)
|
| Budget Amount *help |
¥3,700,000 (Direct Cost: ¥3,700,000)
Fiscal Year 2006: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 2005: ¥2,300,000 (Direct Cost: ¥2,300,000)
|
|---|
| Keywords | TARSH / Abi3bp / Lung cancer / Cellular senescence / mRNA expression / Knockdown / Proliferation / 定量PCR |
|---|
| Research Abstract |
TARSH (Target of NESH-SH3) /Abi3bp was originally isolated as a novel target of NESH-SH3, a member of E3B1/ArgBP/Avi2/NESH, by yeast two-hybrid system and its molecular mechanisms is still unknown. We have already identified mTARSH as a cellular senescence related gene because of its robust induction in the early phase of mouse embryonic fibroblasts (MEFs) cellular senescence. Recent studies have shown that cellular senescence functioned as the tumor suppression mechanism. We have studied about the expression pattern and molecular function of TARSH focusing on the relation between cellular senescence and lung caner. In this study we found that 1) TARSH was specifically expressed in both of mouse and human lung, 2) the expression of this gene was significantly reduced in 15 lines of human lung cancer cell and 80 specimens of primary lung tumor, whereas it predominantly expressed in normal lung tissue, 3) knockdown of TARSH mRNA expression by using short hair-pin RNA caused the growth inhibition, binucleation and aberrant number of centrosomes in MEFs. These evidences suggest that TARSH is involved in both cellular senescence and preventing development cancer and plays an important role in cell cycle progression.
|
