Fractalkine-CX3CR1 axis regulates tumor cell cycle and deteriorates prognosis after radical resection for hepatocellular carcinoma
Fractalkine-CX3CR1 axis regulates tumor cell cycle and deteriorates prognosis after radical resection for hepatocellular carcinoma
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DOI：
10.1002/jso.20642
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发表时间：
2007-03-01
影响因子：
2.5
通讯作者：
Nagasue, Naofumi
中科院分区：
文献类型：
--
作者：
Matsubara, Takeshi;Ono, Takashi;Nagasue, Naofumi
背景和目标：Fractalkine是唯一的CX 3C趋化因子，其受体CX 3CR 1在NK细胞、CD 8 + T细胞、单核细胞和树突状细胞（DC）上表达。尽管研究已经报道了Fractalkine调节宿主免疫应答，但Fractalkine-CX 3CR 1轴在肿瘤生物学和肝细胞癌（HCC）的临床结果中的作用仍然未知。检测Fractalkine和CX 3CR 1在HCC中的表达，并与临床病理特征进行比较，包括增殖细胞核抗原（PCNA）抗体测定的肿瘤进展和手术后患者预后。Fractalkine和CX 3CR 1高表达的肿瘤肝内和肝外复发明显较少，PCNA标记指数（PCNALI）低，组织学分级不同。两种表达的肿瘤患者在无病生存期（DFS）和总生存期（OAS）方面的预后明显更好，这一发现在多变量分析中被确定为独立的预后因素之一。我们的结果表明，Fractalkine-CX 3CR 1轴在肝癌患者的预后中发挥着关键作用，这可能源于已知的宿主免疫反应的调节，和细胞周期的变化。
Background and Objectives: Fractalkine is the only CX3C chemokine, and its receptor, CX3CR1, is expressed on NK cells, CD8+ T cells, monocytes, and dendritic cells (DC). Although studies have reported that fractalkine regulates the host immune response, the roles of the fractalkine-CX3CR1 axis in tumor biology and the clinical results of hepatocellular carcinoma (HCC) remain unknown.Methods: Fractalkine and CX3CR1 expression in HCC were evaluated and compared with the clinicopathologic features, including tumor progression determined by proliferating cell nuclear antigen (PCNA) antibody and patient prognosis after surgery.Results: Tumors with high expression of both fractalkine and CX3CR1 had significantly fewer intra- and extrahepatic recurrences, a low PCNA labeling index (PCNALI), and different histological grades. Patients with tumors that expressed both had a significantly better prognosis in terms of disease-free (DFS) and overall survival (OAS), and this finding was identified as one of the independent prognostic factors in the multivariate analysis.Conclusions: Our results suggest that the fractalkine-CX3CR1 axis plays a pivotal role in the prognosis of patients with HCC, which might arise from the known modulation of the host immune response, and that of the cell cycle in HCC.