Functional analysis of p68 in hepatoma cells and hepatoma vascular endothelial cells

2023 Fiscal Year Final Research Report

• Project/Area Number: 20K08392
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Review Section: Basic Section 53010:Gastroenterology-related
• Research Institution: Nagoya City University
• Principal Investigator: Nojiri Shunsuke 名古屋市立大学, 医薬学総合研究院(医学), 教授 (50381843)
• Co-Investigator(Kenkyū-buntansha): 三浦 裕 至学館大学, 健康科学部, 教授 (90285198)
• Project Period (FY): 2020-04-01 – 2024-03-31
• Keywords: p68 / AFP / 肝癌

Outline of Final Research Achievements

This study attempts to elucidate the biological characteristics of liver cancer from the molecular medical aspect. p68 discovered by the authors is originally recognized to be expressed in the blood vessel of the whole-body continuously, and it seems to be an indispensable gene for the angiogenesis. We discovered that p68 expression acts as a suppressor of alpha-fetoprotein (AFP), which indicates the malignancy of liver cancer. However, the action was completely unknown including the role in the vascular endothelial cell.　From the experiment of KO mouse, p68 is normally expressed in hepatocytes and the malignancy of hepatoma is increased by the inhibition of the p68 expression, and it becomes a carcinogenicity.
Simultaneously, AFP expression rose by the lowering of p68, and it became the molecular medicine proof of the mechanism in which the malignancy was clinically indicated AFP.

Free Research Field

肝臓

Academic Significance and Societal Importance of the Research Achievements

肝臓癌での治療はまだまだ不十分でありその悪性度の生物学的機序も不明であった。今回の実験結果は肝癌の悪性度及び発癌性の一因にｐ６８が関与している事を細胞実験、ヒト臨床検体、さらにＫＯマウスの作製により証明し、腫瘍マーカーであるＡＦＰ上昇メカニズムとの整合性を説明可能とした。今回の研究成果により新たな分子医学的治療への一助になることを期待する。