Establishment of new subtype of so called the triple negative breast cancer from analysis of cancer stem cell and epithelial mesenchymal transition in breast cancer.
| Project/Area Number |
25861152
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
General surgery
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| Research Institution | University of Yamanashi |
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Principal Investigator |
INOUE Ayako 山梨大学, 総合研究部, 病院助教 (60570265)
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2013: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | HER2 / triple negative乳癌 / MHC Class I / T細胞 / siRNA / MAPK / PD98059 / MHC ClassⅠ / トリプルネガティブ乳癌 / 乳癌サブ分類 / 上皮間葉転換 / 癌幹細胞 |
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| Outline of Final Research Achievements |
Immunotherapeutic interventions with T cell-based approaches is targeting HER2. HER2-overexpressing tumors may escape cytotoxic T lymphocyte-mediated lysis by down regulating MHC Class I. We explored expression of HER2, MHC Class I by immunohistochemistry and analyzed their correlation. We also explored the components of the signal transduction pathway that are involved in the regulation of MHC Class I expression using siRNAs targeting HER2 as well as an inhibitor of HER2 signaling. HER2 expression in breast cancers correlated inversely with MHC Class I expression. HER2 depletion by siRNAs resulted in MHC Class I up regulation. Moreover, MHC Class I expression on breast cancer cell lines was upregulated by inhibitor of mitogen-associated protein kinases, in a dose-dependent manner. Thus, agents that target the MAPK signaling pathway may increase MHC Class I expression in breast cancer cells.
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Report
(3 results)
Research Products
(6 results)
