The antibetic drug metformin inhibits esophageal adenocarcinoma cell proliferation in vitro and in vivo.

2014 Fiscal Year Final Research Report

• Project/Area Number: 25860540
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Gastroenterology
• Research Institution: Kagawa University
• Principal Investigator: KOBAYASHI Mitsuyoshi 香川大学, 医学部附属病院, 協力研究員 (70423431)
• Project Period (FY): 2013-04-01 – 2015-03-31
• Keywords: マイクロRNA / 癌増殖抑制 / メトフォルミン / バレット食道腺癌

Outline of Final Research Achievements

Metformin inhibited the proliferation of the esophageal adenocarcinoma cell lines OE19, OE33, SK-GT4 and OACM 5.1C, blocking the G0 to G1 transition in the cell cycle. This was accompanied by strong reductions in G1 cyclins, especially cyclin D1, cyclin-dependent kinase (Cdk)4, and Cdk6, and decreases in retinoblastoma protein phosphorylation. In addition, metformin reduced the phosphorylation of epidermal growth factor receptor and insulin-like growth factor and insulin-like growth factor-1 receptor, as well as angiogenesis-related proteins, such as vascular endothelial growth factor, tissue inhibitor of metalloproteinases (TIMP)-1, and TIMP-2. Metformin also markedly altered microRNA expression. Treatment with metformin of athymic nude mice bearing xenograft tumors reduced tumor proliferation. These findings suggest that metformin may have clinical use in the treatment of esophageal adenocarcinoma.

Free Research Field

消化器内科学