The role of MED12 expression in molecular mechanism of drug resistance of colorectal cancer

2017 Fiscal Year Final Research Report

• Project/Area Number: 15K10130
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Digestive surgery
• Research Institution: Niigata University
• Principal Investigator: Yoshifumi Shimada 新潟大学, 医歯学系, 助教 (20706460)
• Co-Investigator(Kenkyū-buntansha): 坂田 純 新潟大学, 医歯学系, 講師 (70447605) ; 味岡 洋一 新潟大学, 医歯学系, 教授 (80222610) ; 亀山 仁史 新潟大学, 医歯学系, 准教授 (40626420) ; 小杉 伸一 新潟大学, 医歯学総合病院, 特任教授 (90401736) ; 小林 隆 新潟大学, 医歯学総合病院, 講師 (40464010)
• Co-Investigator(Renkei-kenkyūsha): WAKAI Toshifumi 新潟大学, 医歯学系, 教授 (50372470)
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: MED12 / 大腸癌 / 転写メディエーター

Outline of Final Research Achievements

MED12 is a transcriptional mediator complex subunit, which negatively regulates transforming growth factor-β (TGF-β) pathway. TGF-β pathway plays a main role of induction signals of epithelial mesenchymal transition (EMT). We aimed to investigate the clinical significance of MED12 expression in patients with colorectal cancer (CRC). A total of 100 patients diagnosed with stage I-IV CRC were enrolled. MED12 expression was evaluated using immunohistochemistry. The relationships between MED12 loss and clinicopathological characteristics were analyzed. In 100 patients, 79 and 21 patients were classified into MED12 positive and MED12 negative, respectively. MED12 negative was significantly associated with tumor budding, nodal metastasis, and distant metastasis. In conclusion, MED12 loss induces activation of TGF-β pathway resulting EMT. In future, treatment strategy for patients with MED12 loss may improve the prognosis of patients with CRC.

Free Research Field

消化器外科