2011 Fiscal Year Final Research Report
Roles of SIX3 and SIL in the Hedgehog signaling during pancreatic carcinogenesis.
| Project/Area Number |
21590408
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Human pathology
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| Research Institution | Aichi Medical University |
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Principal Investigator |
KASAI Kenji 愛知医科大学, 医学部, 准教授 (70242857)
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| Co-Investigator(Renkei-kenkyūsha) |
IKEDA Hiroshi 愛知医科大学, 医学部, 教授 (00131219)
INAGUMA Shingo 愛知医科大学, 医学部, 講師 (80410786)
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| Project Period (FY) |
2009 – 2011
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| Keywords | ヘッジホッグ / 膵臓癌 / 前癌病変 / SIX3 / SIL |
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| Research Abstract |
SIX3 protein was expressed in the normal duct cells of the pancreas whereas not in PanIN/cancer cells. Human SIX3 promoter contained a CpG island which was methylated in SIX3(-) pancreatic cancer cell lines. Reporter assay revealed roles of SIX3 and TLE1/HDAC1 in the MACS1-dependent suppression of human Shh gene. SIL was strongly expressed in PanIN/cancer cells of the pancreas. It was also weakly expressed at the basal of the normal duct cells of the pancreas, indicating its role for the cellular attachment to the matrix.
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