| Project/Area Number |
24591909
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
General surgery
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| Research Institution | Kumamoto University |
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Principal Investigator |
YAMAMOTO YUTAKA 熊本大学, 医学部附属病院, 特任准教授 (20398217)
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| Co-Investigator(Kenkyū-buntansha) |
IBUSUKI Mutsuko 熊本大学, 大学院生命科学研究部, 助教 (30448526)
IWASE Hirotaka 熊本大学, 大学院生命科学研究部, 教授 (40211065)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2012: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | MACC1 / ｃMet / 乳癌 / 予後因子 / 転写因子 / Breast cancer / c－Met / c-Met |
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| Outline of Final Research Achievements |
MACC1 is suggested to be a transcriptional regulator of cMet, leading to cancer progression and metastasis in colorectal cancer (CRC). So far, the role of MACC1 in breast cancer (BC) has scarcely been investigated. Here, we report its impact on the survival for BC patients and biological function in the cell lines. Reduced MACC1 expressions were associated with BC patient’s mortality. In the cell lines, MACC1 expression was much higher in CRC cells than BC cells. In MACC1 transfected cells, MACC1 overexpression did not induce cMet expression in BC cells, whereas corresponding cMet expression was slightly upregulated in CRC cells. Moreover, the binding of MACC1 to the cMet promoter was suggested in CRC cells, but not in BC cells by ChIP assay. Our findings provide some novel insights into the role of MACC1 for BC, as it was inconsistent with previous studies. There is possibility that MACC1 would not modulate cMet signaling as a transcriptional factor for BC.
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