Molecular mechanism on the basis of morphological atypia in cancer cells

2014 Fiscal Year Final Research Report

• 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
• 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

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.

Free Research Field

病理学