Identification of novel EZH2 mechanism and its network in cancer cells

2016 Fiscal Year Final Research Report

• Project/Area Number: 26430136
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Tumor biology
• Research Institution: Nagoya City University
• Principal Investigator: SHINJO Keiko 名古屋市立大学, 大学院医学研究科, 助教 (40641618)
• Co-Investigator(Renkei-kenkyūsha): KONDO Yutaka 名古屋市立大学, 大学院医学研究科, 教授 (00419897)
• Project Period (FY): 2014-04-01 – 2017-03-31
• Keywords: EZH2 / IKBKE

Outline of Final Research Achievements

Enhancer of zeste homologue 2 (EZH2) is overexpressed in many types of cancer and associated with poor prognosis. However, the underlying mechanism of EZH2 overexpression is not fully understood. Using an EZH2 promoter inhibition assay with an siRNA library targeting known human kinases in colorectal cancer cell lines, we identified a novel role for the IKBKE－NF-κB pathway in upregulating EZH2 expression. IKKe a kinase, was observed to be highly expressed in colorectal cancer tissue. Further validation revealed that inhibiting IKBKE caused a significant reduction in EZH2 expression. These data suggest that the IKKe;－NF-κB pathway may play an important role in regulation of EZH2 expression in colorectal cancer.

Free Research Field

がんエピジェネティクス