Molecular mechanism on the basis of morphological atypia in cancer cells

Research Project

Project/Area Number	24659276
Research Category	Grant-in-Aid for Challenging Exploratory Research
Allocation Type	Multi-year Fund
Research Field	Laboratory medicine
Research Institution	Osaka University
Principal Investigator	NAGUMO Sachiko 大阪大学, 医学(系)研究科(研究院), 特任教授 (80537069)
Co-Investigator(Kenkyū-buntansha)	MATSUURA Nariaki 大阪大学, 大学院医学系研究科, 特任教授 (70190402) KAWAGUCHI Naomasa 大阪大学, 大学院医学系研究科, 准教授 (70224748) MORI Seiji 大阪大学, 大学院医学系研究科, 特任准教授 (90467506)
Project Period (FY)	2012-04-01 – 2015-03-31
Project Status	Completed (Fiscal Year 2014)
Budget Amount *help	¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000) Fiscal Year 2014: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000) Fiscal Year 2013: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000) Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Keywords	病理診断 / 異型性 / インテグリン / カドヘリン / ヒストン修飾 / LINC complex / 細胞異型
Outline of Final Research Achievements	Morphological atypia is classified into structural and cellular atypia. We showed that structural atypia is intimately associated with the alteration of expression levels of adhesion molecules cadherins and integrins. As for cellular atypia, upregulation of H3K9me3 and HP1a is found in the cancer cells with high grade atypia. Interestingly cancer cells with increased expression of H2K9me3 reveal elevated migration and invasion activities in vitro. Regarding LINC (Linkers of the nucleoskeleton to the cytoskeleton) complex molecules, expression levels of SUN1, SUN2 and Nesprin 2 are decreased in cancer cells with high grade atypia.