| Project/Area Number |
12671656
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Otorhinolaryngology
|
|---|
| Research Institution | Fukui Medical University |
|---|
Principal Investigator |
OHTSUBO Toshio Fukui Medical University, Dept. of Otolayngolo Assistant Professor, 医学部・附属病院, 講師 (10223877)
|
|---|
| Project Period (FY) |
2000 – 2001
|
| Project Status |
Completed (Fiscal Year 2001)
|
| Budget Amount *help |
¥4,000,000 (Direct Cost: ¥4,000,000)
Fiscal Year 2001: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2000: ¥2,900,000 (Direct Cost: ¥2,900,000)
|
|---|
| Keywords | Bax / Hyperthermia / Apoptosis / bax / アポトーシス / ハイパーサーミア / 頭頚部腫瘍 / 低pH |
|---|
| Research Abstract |
To investigate the role of bax gene expression in modulating thermosensitivity through an apoptosis-related mechanism, we examined the thermosensitivity and apoptosis after heating in a human head and neck cancer cells (IMC-3 cell lines) transfected with bax gene-bearing mammalian expression vector. Cellular thermosensitivity was determined using the clonogenic assay. Apoptosis was assessed on the basis of the occurrence of apoptotic cells, DNA fragmentation and poly(ADP-ribose)polymerase (PARP) cleavage. Overexpression of the bax gene in IMC-3 cells enhanced thermosensitivity compared with parent cells. The induction of apoptotic cells, DNA fragmentation and PARP cleavage in bax transfected IMC-3 cells were more prominent than those in IMC-3 cells. These findings suggest that bax contributes to thermosensitization by enhancing the induction of haat-induced apoptosis.
|
