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

通过趋化因子受体研究肝癌转移和生长的机制

• 批准号: 18590743
• 负责人: ITOH Yoshito
• 金额: $ 2.36万
• 依托单位: Kyoto Prefectural University of Medicine
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2006
• 资助国家: 日本
• 起止时间: 2006 至 2007
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-18590743/
• 关键词: HCC; chemokine; chemokine receptor; metastasis; growth; signal transduction; 肝癌

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.

我们用真实的时间PCR检测了肝癌细胞系趋化因子受体的表达。CXC趋化因子受体CXCR 4在PLC/PRF/5细胞上强表达，CC趋化因子受体CCR 6在HuH 7、Al和HepG 2细胞上强表达，CXCR 4的配体SDF-1由PLC/PRF/5细胞分泌，CCR 6的配体MIP-3 α由HuH 7、Al和HepG 2细胞分泌，向HuH 7细胞的培养基中添加MIP-3 α增加了体外活HuH 7细胞的数量。根据这些结果，我们推测一定数量的HCC细胞的生长归因于HCC细胞和淋巴细胞在发炎的人肝脏中分泌的增加的趋化因子。趋化因子及其受体系统可能通过旁分泌或自分泌方式参与肝癌的生长。我们还使用表达CXCR 4的Al细胞系进行了实验，但我们无法发现该系统实际上在这种情况下起作用。