2015 Fiscal Year Final Research Report
The development of the epithelial-mesenchymal transition invasion and metastasis suppressive therapy of choroidal malignant tumor that target
Project/Area Number |
23592583
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Ophthalmology
|
Research Institution | Wakayama Medical University |
Principal Investigator |
TANAKA SAIICHI 和歌山県立医科大学, 医学部, 講師 (60316106)
|
Co-Investigator(Kenkyū-buntansha) |
SAIKA SHIZUYA 和歌山県立医科大学, 医学部, 教授 (40254544)
|
Co-Investigator(Renkei-kenkyūsha) |
Okada Yuka 和歌山県立医科大学, 医学部, 准教授 (50264891)
|
Project Period (FY) |
2011-04-28 – 2016-03-31
|
Keywords | 悪性黒色腫 / 上皮間葉系移行 |
Outline of Final Research Achievements |
Local invasion or metastasis of neoplastic cells derived from choroidal malignant melanoma reportedly depends on epithelial-mesnechymal transition (EMT), that is promoted by a growth factor, transforming growth factor b (TGFb). In cell culture study adding TGFb1 (1 ng/ml) activates Smad2/3 and p38 signals, but not Erk and JNK signals. Phosphorylated proteins of Smad2/3 and p38 were detected both in the cytoplasm and nuclei of B16 cells. Observation of expression pattern of EMT markers indicated that adding exognosus TGFb1 accelerated expression of collagen type I and vimentin, but not alpha-smooth muscle actin and fibronectin, suggesting TGFb1 promotes partial EMT in B16 cells. Exposure to TGFb1 did not induce cell death, although TGFb1 reportedly induces apoptosis or cell proliferation inhibition in neoplastic epithelial cell types. Modulating TGFb1-related signals and resultant EMT process could be beneficial in improving prognosis of the patients with choroidal malignant melanoma
|
Free Research Field |
眼科
|