| Project/Area Number |
10470333
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (B)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Urology
|
|---|
| Research Institution | NIIGATA UNIVERSITY |
|---|
Principal Investigator |
TOMITA Yoshihiko Faculty of Medicine, NIIGATA UNIVERSITY associate, 医学部, 助教授 (90237123)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
TANIKAWA Toshiki University Hospital, NIIGATA UNIVERSITY Lecturer, 医学部・附属病院, 講師 (70236686)
斉藤 俊弘 新潟大学, 医学部附属病院, 助手 (40251813)
|
|---|
| Project Period (FY) |
1998 – 1999
|
| Project Status |
Completed (Fiscal Year 1999)
|
| Budget Amount *help |
¥10,700,000 (Direct Cost: ¥10,700,000)
Fiscal Year 1999: ¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1998: ¥8,600,000 (Direct Cost: ¥8,600,000)
|
|---|
| Keywords | renal cell cancer / bcl-2 / antisense oligonucleotide / gene therapy / アンチセンスオリゴDN4 / アポトーシス |
|---|
| Research Abstract |
We have previously shown that Bcl-2 expression was negative prognostic factor in transitional cell cancer (TCC), and that TCC cell lines expressing high levels of Bcl-2 are resistant to Adriamycin triggered apoptosis. Here we examined antisense oligonucleotide - mediated downregulation of Bcl-2 expression and its effect on sensitivity to ADM treatment in T24 cells. Treatment of T24 cells with 20 μM of bcl-2 antisense PODN reduced the Bcl-2 protein level. Combined administration with Adriamycin resulted in synergistic cytotoxicity, accompanied with a 2.4-fold increase in DEVD-specific caspase activity. The finding provides evidence that Bcl-2 expression may be critical for maintaining the drug resistance of TCC. bcl-2 antisense PODN might be useful means for. overcoming drug resistance in highly malignant TCC,
|
