Investigation of the biological characteristics of hepatocellular carcinoma arising from NAFLD and searching for novel therapeutic targets.

2021 Fiscal Year Final Research Report

• Project/Area Number: 19K16739
• Research Category: Grant-in-Aid for Early-Career Scientists
• Allocation Type: Multi-year Fund
• Review Section: Basic Section 50010:Tumor biology-related
• Research Institution: Hamamatsu University School of Medicine
• Principal Investigator: Takeda Makoto 浜松医科大学, 医学部, 助教 (50839157)
• Project Period (FY): 2019-04-01 – 2022-03-31
• Keywords: 肝細胞癌 / 非アルコール性脂肪肝疾患 / スフィンゴシン１リン酸 / S1PR2

Outline of Final Research Achievements

S1PR2 expression in three human hepatocellular carcinoma lines (HLE, HepG2, and HuH7) was confirmed by western blot analysis, and S1PR2 expression was HLE=HepG2>HuH7. S1PR2 knockdown demonstrated inhibition of cell proliferation by S1P.
OA-induced proliferation was inhibited by the addition of JTE013 and S1PR2KD when oleic acid (OA) was added. S1P in the culture supernatant fluid was increased by by S1PR2KD, indicating that the S1P-S1PR2 pathway is involved in the proliferation mechanism of HCCs in the background of NAFLD.

Free Research Field

肝胆膵悪性腫瘍

Academic Significance and Societal Importance of the Research Achievements

近年、メタボリックシンドロームに伴う非アルコール性脂肪肝疾患（NAFLD)を背景とするHCCが増加してきており、その生物学的特徴の解明は急務である。本研究成果は、その生物学的特徴を脂質の観点から解明したものであり、新たな治療展開を期待できるものと考える。同時に、HCCだけではなく他癌種においても脂質が治療標的となる可能性があると考えられる。