Downstream of newly identified transcriptional repressor and its role in the progression of non-invasive breast cancer.
Project/Area Number |
15K08358
|
Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Human pathology
|
Research Institution | Aichi Medical University |
Principal Investigator |
KASAI KENJI 愛知医科大学, 医学部, 教授 (70242857)
|
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)
ITO HIDEAKI 愛知医科大学, 医学部, 助教 (90711276)
|
Project Period (FY) |
2015-04-01 – 2018-03-31
|
Project Status |
Completed (Fiscal Year 2017)
|
Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2017: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2016: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2015: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
|
Keywords | 乳癌 / 遺伝子制御 / Hedgehog / TSHZ2 / FAM64A / DCIS / 転写抑制因子 / 標的遺伝子 / クロマチン制御 / DNA複製 |
Outline of Final Research Achievements |
I identified TSHZ2 as a down-regulated gene during breast carcinogenesis. TSHZ2 was found to make a ternary complex with GLI1 and CtBP2 in the nucleus of normal duct epithelium and suppress the target gene expression of GLI1. This indicates that down-regulated TSHZ2 and in turn up-regulated target genes of GLI, such as CXCR4 and AEBP1, would be responsible for breast cancer progression. I next identified FAM64A, FAM83D, DLGAP5, FOXM1 and DONSON as candidates of TSHZ2 target genes. Especially, I found that FAM64A associates with several nuclear proteins which are involved in chromatin remodeling and DNA replication.
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Report
(4 results)
Research Products
(5 results)