Functional and clinical analysis of angiogenic factor apelin in hepatocellular carcinoma

2014 Fiscal Year Final Research Report

• Project/Area Number: 24592005
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Digestive surgery
• Research Institution: Kyushu University
• Principal Investigator: SUGIMACHI Keishi 九州大学, 大学病院, 特別教員 (90452763)
• Co-Investigator(Kenkyū-buntansha): SHIRABE Ken 九州大学, 医学(系)研究科(研究院), 准教授 (70264025) ; MAEHARA Yoshihiko 九州大学, 医学(系)研究科(研究院), 教授 (80165662) ; EGUCHI Hidetoshi 九州大学, 大学病院, 講師 (90527756) ; IGUCHI Tomohiro 九州大学, 大学病院, 助教 (30598959) ; AKIYOSHI Sayuri 九州大学, 大学病院, 助教 (50567360) ; SUDO Tomoya 九州大学, 大学病院, 助教 (50309803)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: 肝細胞癌 / 血管新生 / アペリン / F13A / CD34

Outline of Final Research Achievements

The aim of this study was to clarify the role of the apelin-APJ system which regulates angiogenesis in tumor progression of hepatocellular carcinoma (HCC). Expressions of angiogenic factors and vascular markers were investigated in specimens from 90 HCC patients. A subcutaneous HCC tumor mouse model was treated with the APJ antagonist, F13A, and tumor growth and vascular development were assessed. APJ expression was observed in arteriole-smooth muscle. Higher amounts of APJ+-arteriole and apelin were detected in tumors (p<0.001 for both). APJ+-arteriole and apelin expression were more commonly observed in moderately- and poorly-differentiated than in well-differentiated HCC (p=0.003). HCC with irregular dilated arteries expressed higher levels of apelin (p=0.012). Tumor growth was inhibited by treatment with F13A (p<0.001), and arterioles were decreased in the treated group (p=0.047), in vivo. Apelin-APJ is overexpressed, and works as a signal for arteriogenesis in HCC.

Free Research Field

消化器外科、肝胆膵外科