| Project/Area Number |
25870093
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Experimental pathology
Tumor biology
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| Research Institution | University of Tsukuba |
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Principal Investigator |
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| Project Period (FY) |
2013-04-01 – 2015-03-31
|
| Project Status |
Completed (Fiscal Year 2014)
|
| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2013: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 腫瘍形成 / TMEPAI / 発現制御 / TGF-beta / EGF / 癌関連遺伝子 / がん / TGF-b/Smad |
|---|
| Outline of Final Research Achievements |
TMEPAI is a type I transmembrane protein which is highly expressed in diverse cancer cells. We previously reported that TMEPAI inhibits TGF-b signaling pathway. However, TMEPAI’s role in cancer cell was poorly understood. First, we established TMEPAI knock-down model using lung carcinoma cells, then performed xenograft assay and in vitro sphere formation assay. As a result, Knock-down of TMEPAI significantly reduces lung tumorigenesis emphasizing that autocrine TGF-b is essential for the high expression of TMEPAI in lung carcinoma. Furthermore, EGF signaling collaboratively regulates TGF-b-induced TMEPAI expression. Additionally, C18orf1, a family molecule of TMEPAI, also suppresses TGF-b signaling.
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