The mechanism of tumorigenesis by disruption of the regulation of geminin proteolysis

2014 Fiscal Year Final Research Report

• Project/Area Number: 25670778
• Research Category: Grant-in-Aid for Challenging Exploratory Research
• Allocation Type: Multi-year Fund
• Research Field: Morphological basic dentistry
• Research Institution: The University of Tokushima
• Principal Investigator: KUDO Yasusei 徳島大学, ヘルスバイオサイエンス研究部, 准教授 (50314753)
• Project Period (FY): 2013-04-01 – 2015-03-31
• Keywords: geminin / ユビキチン分解 / 癌化

Outline of Final Research Achievements

In this study, we examined the relationship between overexpression of Geminin protein due to abnormal regulation of ubiquitin-mediated proteolysis and tumorigenesis. Stabilized Geminin by phosphorylation on Thr25 inhibited pre-replication complex formation via inhibition of Cdt1 loading to chromosome at G1 phase. Overexpression of Gemini protein by abnormal regulation of Thr25 phosphorylation was not observed in cancer cells, but constitutive phosphorylation on Thr25 was observed in some cancer cells. Thus, we investigated how overexpression of geminin protein via prevention from ubiquitin-mediated proteolysis caused by constitutive Thr25 phosphorylation contribute to tumorigenesis.

Free Research Field

口腔病理学