Calponin h1-gene therapy using Tat-peptide vector against peritoneal dissemination of ovarian cancer

2014 Fiscal Year Final Research Report

• Project/Area Number: 24592520
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Obstetrics and gynecology
• Research Institution: Kagoshima University (2014); Kyushu University (2012-2013)
• Principal Investigator: KOBAYASHI Hiroaki 鹿児島大学, 医歯(薬)学総合研究科, 准教授 (70260700)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: カルポニンh1 / アクチン / 細胞骨格蛋白質 / 卵巣癌 / 癌性腹膜炎 / 分子標的治療 / Taｔペプチド / 膜透過性ペプチド

Outline of Final Research Achievements

Objectives: Actin binding protein calponin h1 (CNh1) stabilizes cytoskeletal actin. We tried to identify the responsibility site in actin stabilization which can be a molecular target for ovarian cancer therapy. Methods: The full length or several mutant form of CNh1 were constructed and introduced into ovarian cancer cell lines. Immunocytochemistry was performed to evaluate the localization of transfected CNh1 and the level of actin polymerization. The growth, migration and invasion ability of transfected cells were also measured. Results: The ratio of actin polymerization was revealed as follows: 73% in CNh1 full length transfection; 66% in calponin repeat structure (CNR1); 36% in mock transfection. The cell morphology changed depending on the actin polymerization. The growth, migration and invasion ability were significantly suppressed in both CNh1 full length and CNR1 introduced cells.
Conclusion: CNR1 was suggested to become a molecular target for ovarian cancer therapy.

Free Research Field

婦人科悪性腫瘍