Investigation of microRNA interaction between pancreatic cancer cells and the stromal cells aiming to overcome the resistance to chemotherapeutic drugs.

2015 Fiscal Year Final Research Report

• Project/Area Number: 25462111
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Digestive surgery
• Research Institution: Osaka University
• Principal Investigator: Eguchi Hidetoshi 大阪大学, 医学(系)研究科(研究院), 准教授 (90542118)
• Co-Investigator(Kenkyū-buntansha): WADA Hiroshi 大阪大学, 大学院医学系研究科, 助教 (00572554) ; HAMA Naoki 独立行政法人国立病院機構, 大阪医療センター(臨床研究センター), 研究員 (00645723) ; NAGANO Hiroaki 山口大学, 医学系研究科, 教授 (10294050) ; KAWAMOTO Kouichi 大阪大学, 大学院医学系研究科, 助教 (30432470) ; KOBAYASHI Syougo 地方独立行政法人大阪府立病院機構, 大阪府立成人病センター, その他 (30452436) ; HASEGAWA Shinichirou 大阪大学, 医学部付属病院, その他 (60621026) ; AKITA Hirofumi 地方独立行政法人大阪府立病院機構, 大阪成人病センター, その他 (70528463)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: microRNA / 癌間質 / エクソソーム

Outline of Final Research Achievements

We established gemcitabine-resistant pancreatic cancer cells, and miR-320c was selected as a responsible miRNA for the drug-resistance by microarray analysis between the resistant cells and its parental cells. Among the target genes for miR-320c, SMARCC1 was investigated by immunohistochemistry, and was shown to have a positive correlation to a better survival.
Exosomes derived from pancreatic cancer cells cultured in a hypoxic condition was added to human dermal fibroblasts (HDFs), and the expression level of α-SMA in HDFs was more obviously increased than the exosomes derived from cells cultured in normal condition. Moreover, the addition of HDFs with increased α-SMA to another pancreatic cancer cells has shown to increase the growth rate and invasiveness.

Free Research Field

消化器外科学