2014 Fiscal Year Final Research Report
AhR signaling suppresses tumor progression and metastatic potential of breast cancer cells by inducing ubiquitin ligase CHIP.
| Project/Area Number |
25893022
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
Biological pharmacy
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| Research Institution | University of Tsukuba |
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Principal Investigator |
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| Project Period (FY) |
2013-08-30 – 2015-03-31
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| Keywords | 乳がん / AhR |
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| Outline of Final Research Achievements |
Breast cancer has poor survival and high recurrence rates for aggressive metastatic disease. There is no preferred agent for metastasis of breast cancer. In this study, I show that aryl hydrocarbon receptor (AhR) ligand, YL-109 has ability to inhibit breast cancer cell growth and invasiveness in vitro and in vivo. YL-109 increased the expression of carboxyl terminus of Hsp70-interacting protein (CHIP), which suppresses tumorigenic and metastatic potential of breast cancer cells. YL-109 induced CHIP transcription because of the recruitment of the AhR to upstream of CHIP gene in breast cancer cells. Consistently, the antitumor effects of YL-109 were depressed by CHIP or AhR knockdown in breast cancer cells. Taken together, my findings indicate that a novel agent YL-109 inhibits cell growth and metastatic potential by inducing CHIP expression through AhR signaling in breast cancer cells. It suggests that YL-109 is a potential candidate for breast cancer therapy.
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| Free Research Field |
分子生物学
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