Mechansim by which Arf6 protein becomes overexpressed in cancer to promote malignancy

2016 Fiscal Year Final Research Report

• Project/Area Number: 15K15057
• Research Category: Grant-in-Aid for Challenging Exploratory Research
• Allocation Type: Multi-year Fund
• Research Field: General medical chemistry
• Research Institution: Hokkaido University
• Principal Investigator: Sabe Hisataka 北海道大学, 医学研究科, 教授 (40187282)
• Project Period (FY): 2015-04-01 – 2017-03-31
• Keywords: Arf6 / eIF4A / mRNA translation / cancer malignancy

Outline of Final Research Achievements

We have shown previous that the small-GTPase Arf6 and its downstream signaling factors are frequently overexpressed in different cancers and execute a cancer mesenchymal program, including invasion, metastasis and drug resistance. Here, we show a molecular basis by which Arf6 protein becomes overexpressed in some cancer cells. Our results indicated that an oncogenic mutation of a certain gene evokes an enhanced activity of eIF4A, which promotes translation of the Arf6 mRNA; and thus established an causative role of the enhanced mRNA translation in cancer malignancy development.

Free Research Field

分子腫瘍学