Controling cancer development by reprogramming technique

2016 Fiscal Year Final Research Report

• Project/Area Number: 26460468
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Experimental pathology
• Research Institution: Tohoku University
• Principal Investigator: Horii Akira 東北大学, 医学系研究科, 教授 (40249983)
• Project Period (FY): 2014-04-01 – 2017-03-31
• Keywords: 膵がん / がん幹細胞 / リプログラミング / 増殖抑制 / EMT / 薬剤耐性 / 細胞遊走能

Outline of Final Research Achievements

Reprogramming mediated control of pancreatic cancer cell lines were attempted in this study. Four Yamanaka factors were introduced into pancreatic cancer cell lines PK-8 and PK-9 as well as their derived gemcitabine (GEM herein after) resistant cell lines RPK-8 and RPK-9. Lentivirus vector was first used but results were not successful. We next tried TET-vector but results were not successful. However, we observed some unexpected interesting findings. GEM resistance in RPK-9 is caused by homozygous deletion of DCK that is essential for activation of GEM. Hence, RPK-9 can survive under very high concentration of GEM. On the other hand, RPK-8 can survive under low concentration of GEM but cannot survive under very high concentration. Furthermore, upregulation of genes associated with stemness and EMT were evident in RPK-8. Cell motility was also upregulated. These results may suggest that stemness associated with EMT is playing an important role in acquisition of GEM in RPK-8.

Free Research Field

実験病理学