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.

2014 Fiscal Year Final Research Report

• Project/Area Number: 25861152
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: General surgery
• Research Institution: University of Yamanashi
• Principal Investigator: INOUE Ayako 山梨大学, 総合研究部, 病院助教 (60570265)
• Project Period (FY): 2013-04-01 – 2015-03-31
• Keywords: HER2 / triple negative乳癌 / MHC Class I / T細胞 / siRNA / MAPK / PD98059

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.

Free Research Field

乳腺外科学