| Budget Amount *help |
¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2014: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2013: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2012: ¥3,120,000 (Direct Cost: ¥2,400,000、Indirect Cost: ¥720,000)
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| 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.
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