Investigation for the mechanisms of metastasis and growth of HCC via chemokine receptors

• Project/Area Number: 18590743
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Single-year Grants
• Section: 一般
• Research Field: Gastroenterology
• Research Institution: Kyoto Prefectural University of Medicine
• Principal Investigator: ITOH Yoshito Kyoto Prefectural University of Medicine, Graduate School of Medical Science, Lecturer (70244613)
• Project Period (FY): 2006 – 2007
• Project Status: Completed (Fiscal Year 2007)
• Budget Amount: ¥3,690,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥390,000); Fiscal Year 2007: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000); Fiscal Year 2006: ¥2,000,000 (Direct Cost: ¥2,000,000)
• Keywords: HCC / chemokine / chemokine receptor / metastasis / growth / signal transduction / 肝癌

Research Abstract

We investigated the expression of chemokine receptors on HCC cell lines by real time PCR. CXC chemokine receoptor CXCR 4 was strongly expressed on PLC/PRF/5 cells, and CC chemokine receptor CCR6 was strongly expressed on HuH7, Al, and HepG2 cell lines.
The ligand of CXCR4, SDF-1was secreted by PLC/PRF/5 cells, and the ligand of CCR6, MIP-3 alpha was secreted by HuH7, Al, and HepG2 cell lines.
Addition of MIP-3 alpha to the medium of HuH7 cells increased the number of viable HuH7 cells in vitro. From these results, we speculate that the growth of a certain number of HCC cells was attributable to the increased chemokines secreted by HCC cells and lymphocytes in the inflamed lhuman liver. Chemokine and chenokine receptor system may by one of the mechanisms of the growth of HCC in a paracrine or autocrine way..
We also performed experiments using Al cell line which express CXCR4, but we could not find that the system was actually working on this occasion.