New cancer treatment focusing on genetic instability of the cancer stem cell
Project/Area Number |
24659614
|
Research Category |
Grant-in-Aid for Challenging Exploratory Research
|
Allocation Type | Single-year Grants |
Research Field |
Digestive surgery
|
Research Institution | Kyushu University |
Principal Investigator |
MAEHARA Yoshihiko 九州大学, 医学(系)研究科(研究院), 教授 (80165662)
|
Project Period (FY) |
2012-04-01 – 2014-03-31
|
Project Status |
Completed (Fiscal Year 2013)
|
Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
|
Keywords | 染色体不安定性 / 酸化ストレス / BuBR1 / p53 / がん幹細胞 / LgR5 / LGR5 / 遺伝子不安定性 / 癌幹細胞 / CD44 |
Research Abstract |
The cancer stem cell remains to be resistant to the treatment such as chemotherapy or the radiation. We can propose a new treatment to reduce recurrence and metastasis by targetting the cancer stem cell. Because a cancer is exposed to hypoxia and chemical irritation partially, some cells become a stem like cell and become to generate genetic instability. In our experiment,oxidative stress (OS) causes DNA damage and chromosome instability that may lead to carcinogenesis. OS is also suggested to contribute to an increase in aneuploid cells. However, it is not clear how OS is involved in the regulation of SAC and contributes to carcinogenesis associated with aneuploidy. Here we show that an oxidant (KBrO3) activated the p53 signaling pathway and suppressed the expression of SAC factors, BubR1, and Mad2, in human diploid fibroblast MRC5 cells. This suppression was dependent on functional p53 and reactive oxygen species.
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Report
(3 results)
Research Products
(58 results)
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