Suppression of delayed ROS rescue normal human fibroblasts after radiation exposure.
Description: We revealed that radiation induces delayed increase of reactive oxygen species (ROS) in both normal cells and tumor cells. However, delayed ROS is required for induction of cellular senescence only in normal cells but not in tumor cells. We then analysed the expression of proteins related to senescence. The expression of p53 and p21 are increased with delayed ROS in normal cells. Surprisingly, the suppression of delayed ROS did not reduce the expression of p53 in RKO cells, even RKO cells have the wild type p53. We are now exploring the upstream target for delayed ROS.
Amount: ¥3,900,000
Funding type: fellowship
Funder scheme: Grant-in-Aid for Young Scientists (B)
Start date: 2016-04-01
End date: 2019-03-31
Investigator: Shinko Kobashigawa
Institution: Kyoto University(2017-2018)Oita University(2016)
Funded outputs count: 4
Funder award ID: 16K19836
OpenAlex ID: G7149906071