2010 Fiscal Year Final Research Report
The development of the novel treatment that targeted plural cancer specific genes
| Project/Area Number |
20591624
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Digestive surgery
|
|---|
| Research Institution | Nagoya University |
|---|
Principal Investigator |
KOKURYO Toshio Nagoya University, 医学系研究科, 特任助教 (60378023)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
NGINO Masato 名古屋大学, 大学院・医学系研究科, 教授 (20237564)
YOKOYAMA Yukihiro 名古屋大学, 大学院・医学系研究科, 寄附講座講師 (80378091)
UEHARA Keisuke 名古屋大学, 医学部附属病院, 病院助教 (50467320)
|
|---|
| Project Period (FY) |
2008 – 2010
|
| Keywords | Nek2 / TLK1 / FAK |
|---|
| Research Abstract |
The cancer progression is dependent on complicated conditions of cancer specific genes. It is important to target the plural genes for the development of an effective molecule targeted therapy. We performed analysis about cancer specific genes, such as Nek2 (NIMA related kinase 2), FAK (Focal adhesion kinase) and TLK1 (Tousled like kinase 1). The simultaneous suppression of Nek2 and FAK inhibited proliferation and induced apoptosis, compared with single suppression of Nek2 or FAK. The double restraint of Nek2 and TLK1 also inhibited the proliferation and induced apoptosis. The combination treatment of Nek2 siRNA and CDDP increased inhibitory effect in proliferation and cell survival in cancer cell. We identified the over expression of BCL2L1 and APAF-1 (apoptotic protease activating factor 1), the suppression of FOS and JUN in combination treatment. The concomitant usage of TLK1 siRNA and CDDP enhanced apoptosis in comparison with TLK1 siRNA or CDDP treatment.
Our data indicated the combination of siRNA and the anticancer agent may be a novel cancer targeted therapy.
|
