| Project/Area Number |
25640059
|
|---|
| Research Category |
Grant-in-Aid for Challenging Exploratory Research
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Tumor biology
|
|---|
| Research Institution | University of Tsukuba |
|---|
Principal Investigator |
|
|---|
| Co-Investigator(Renkei-kenkyūsha) |
SUZUKI Hiroyuki 筑波大学, 医学医療系, 准教授 (70375509)
|
|---|
| Project Period (FY) |
2013-04-01 – 2015-03-31
|
| Project Status |
Completed (Fiscal Year 2014)
|
| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
|
|---|
| Keywords | 扁平上皮がん / 食道がん / 子宮頸がん / 肺がん / THG-1 / RAS/MAPK経路 / 扁平上皮癌 / がん細胞代謝 / 浸潤 / がん幹細胞 / Keap-1 / Nrf2 |
|---|
| Outline of Final Research Achievements |
TGF-1 is expressed only in the basal layer of stratified squamous epithelia and the elevated expression of THG-1 is commonly observed in squamous cell carcinoma (SCC); such as esophageal cancer, cervical cancer, and lung SCC. It is phosphorylated by ERK in the downstream of epidermal growth factor receptor/Ras/MAPK pathway and essential for the tumorigenic activity of SCC. We also identified downstream target molecules of THG-1 by TOF/MS screening and confirmed the functional significance of these binding proteins in tumorigenic activity by using multiple molecular cell biological experiments. Mutations of the phosphorylation site or binding motifs to the downstream effectors abrogated the tumorigenic function of THG-1. These findings indicated that THG-1 is a novel tissue-specific oncogene of SCC.
|
