Basic study of the treatment with anti-survivin and heavy ion radiotherapy for drug-resistant kidney and prostate cancer.

2015 Fiscal Year Final Research Report

• Project/Area Number: 25462467
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Urology
• Research Institution: Gunma University
• Principal Investigator: KOIKE Hidekazu 群馬大学, 医学部附属病院, 講師 (90420091)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: サバイビン / 腎癌

Outline of Final Research Achievements

We induced a rapamycin-resistant clear cell carcinoma cell line (Caki-1-RapR). We showed that survivin gene expression was significantly up-regulated in Caki-1-RapR compared with that in its parent cells (Caki-1). Caki-1-RapR cells had significantly more invasion ability than Caki-1 cells in a Matrigel invasion assay and more migration ability in a wound-healing assay. In Caki-1-RapR cells, rapamycin did not up-regulate caspase-9 activity and did not induce apoptosis. In Caki-1-RapR cells, YM155(survivin inhibitor) significantly decreased survivin gene and protein expression levels and cell proliferation in a dose-dependent manner in vitro. In addition, YM155 treatment significantly reversed rapamycin resistance in Caki-1-RapR cells. In a nude mouse tumor xenograft model, YM155 significantly inhibited the growth of Caki-1-RapR tumor. In addition, YM155 significantly enhanced the antitumor effects of rapamycin in Caki-1-RapR tumor.

Free Research Field

泌尿器科学