| 研究実績の概要 |
We worked to find appropriate therapeutic target-enzymes of acetylation or deacetylation of RAd52 in BRCA1/2-dysfunctioned cells (Capan-1, BxPC3,and UWB1-cell line) and control cells. Several candidate enzymes were identified.
First, we examined whether the cell proliferation, viability, and sensitivity to anti-cancer agents of these cells were changed or not by the knock-down of the each candidate enzyme. Next, we have investigated the cell-proliferation and viability of cells with double-knock down of the candidate enzyme and BRCA1/2 by siRNA. We also investigated whether the double knockdown has impacts on he efficacy of homologous recombination induced by irradiation and anti-cancer agents.
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