2010 Fiscal Year Final Research Report

A functional role of Par-4 in endometrial tumorigenesis

Research Project

Project/Area Number	20590352
Research Category	Grant-in-Aid for Scientific Research (C)
Allocation Type	Single-year Grants
Section	一般
Research Field	Human pathology
Research Institution	Kitasato University
Principal Investigator	SAEGUSA Makoto Kitasato University, 医学部, 教授 (00265711)
Project Period (FY)	2008 – 2010
Keywords	Par-4 / 子宮内膜癌 / アポトーシス / 細胞増殖
Research Abstract	Constitutively high levels of Par-4 expression were observed in epithelial cells through the menstrual cycle, in contrast to the transient up-regulation in stromal components in the menstrual stage, positively correlated with the phospho-p65 and apoptosis. Most ECs exhibited significant down-regulation, with positive links only to pp65 expression. Transfection of p65 led to transactivation of Par-4. Overexpression of Par-4 resulted in induction of not only apoptosis but also senescence, through changes in expression of bcl-2 and p21WAF1, respectively. Together, these findings suggest that a signaling cascade involving sequential activation of NF-_κB/p65 and Par-4 may participate in relatively early events of endometrial tumorigenesis, leading to modulation of cell kinetics including apoptosis and cell cycle progression.