The molecular mechanisms and regulation of acquisition of tumor invasive abilities through actin cytoskeleton remodeling

2015 Fiscal Year Final Research Report

• Project/Area Number: 25871074
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Tumor biology; Tumor therapeutics
• Research Institution: Microbial Chemistry Research Foundation (2015); Tokyo Metropolitan Institute of Medical Science (2014); Japanese Foundation for Cancer Research (2013)
• Principal Investigator: OHISHI Tomokazu 公益財団法人微生物化学研究会, 沼津支所, 研究員 (50442546)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: アクチン細胞骨格 / 細胞運動 / 浸潤 / ポリ(ADP-リボシル)化

Outline of Final Research Achievements

In this study, we investigated the function of TAB182, which is a binding protein of poly(ADP-ribose)polymerase tankyrase, and the involvement of TAB182 dysfunction in the regulation of cancer cells migration and invasion. 1) TAB182 depletion activated the ROCK-LIMK pathway, which is overexpressed in various cancer cells, and enhanced cancer cell migration and invasion. Tankyrase overexpression also activated the ROCK-LIMK pathway without depletion of TAB182. 2) To investigate the involvement of TAB182 expression changes in the clinical cancer setting, we performed tissue microarray-based immunohistochemistry. Among various cancers, TAB182 expression was significantly lower in the area of invasion than that of non-invasion in pancreatic cancer.

Free Research Field

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