| Project/Area Number |
26893175
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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 |
Pathological medical chemistry
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| Research Institution | The University of Tokushima |
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Principal Investigator |
KIMURA Ryuichiro 徳島大学, 疾患プロテオゲノム研究センター, 特任助教 (20587323)
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| Project Period (FY) |
2014-08-29 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | 乳癌 / ゲノム / シグナル伝達 / プロテオーム / 発現制御 |
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| Outline of Final Research Achievements |
We investigated the role of brefeldin A-inhibited guanine nucleotide-exchange protein 3 (BIG3) in onset/development mechanism of estrogen receptor (ER)-negative breast cancers, including triple-negative breast cancer (TNBC). BIG3 was highly expressed in ER-negative breast cancer, as well as ER-positive cancer. Notably, BIG3 was strongly expressed in HER2-enriched breast cancer. A mechanism for BIG3 expression in ER-negative breast cancer was different from it in ER-positive breast cancer. High expression of BIG3 was associated with significantly shorter overall survival in both ER-positive and -negative cancer on public cohort. Knockdown of BIG3 expression with small-interfering RNA reduced cellular growths of human TNBC cell lines. Furthermore, we identified novel BIG3-interacting factors in breast cancer cells. These results demonstrate that BIG3 directly regulates cellular survival and growth of TNBC.
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