Macrophage inhibitory factor 1 acts as a potential biomarker in patients with esophageal squamous cell carcinoma and is a target for antibody-based therapy.
Macrophage inhibitory factor 1 acts as a potential biomarker in patients with esophageal squamous cell carcinoma and is a target for antibody-based therapy.
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巨噬细胞抑制因子 1 是食管鳞状细胞癌患者的潜在生物标志物，也是基于抗体的治疗的靶点。
DOI：
10.1111/cas.12331
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发表时间：
2014-02
期刊：
影响因子：
5.7
通讯作者：
Lu SH
中科院分区：
文献类型：
--
作者：
Wang XB;Jiang XR;Yu XY;Wang L;He S;Feng FY;Guo LP;Jiang W;Lu SH
巨噬细胞抑制因子1(MIC1)在多种癌症中经常发生改变。本研究旨在探讨MIC1在食管鳞癌(ESCC)中的临床意义。检测286例ESCC患者和250例健康人血清MIC1，评价其诊断性能，并与SCC、CEA、CA199、CA724进行比较，评价其作为预后指标的价值。检测MIC1在ESCC细胞系、组织中的表达，并在体内外进行MIC1抗体对ESCC的抑制作用。结果表明，食管鳞癌患者血清MIC1水平显著高于正常对照组(P<0.001)，并与肿瘤侵袭(P=0.030)、淋巴结转移(P=0.007)呈正相关。MIC1的敏感性明显高于SCC、CEA、CA199和CA724，尤其对I期ESCC的敏感性更高。血清MIC1水平高的患者在无复发(P=0.050)和肿瘤特异性生存期(P=0.005)方面预后也较差。体外研究表明，MIC1在37.5%(3/8)的食管癌细胞系和45%(18/40)的食管癌组织中表达上调，肿瘤组织中MIC1的转录水平显著高于癌旁正常组织(P=0.001)。MIC1抗体抑制肿瘤生长(P<；0.001)，并在异种移植模型中表现出对肿瘤组织的偏爱。新生血管管腔的形成减少可能是其机制之一。结论：MIC1在食管癌的发生发展中起重要作用，可作为食管癌的潜在生物标志物和治疗靶点。
Macrophage inhibitory factor 1 (MIC1) is frequently altered in various cancers. The aim of this study was to investigate the clinical significance of MIC1 for esophageal squamous cell carcinoma (ESCC). Serum MIC1 of 286 ESCC and 250 healthy subjects was detected, the diagnostic performance was assessed and compared with SCC, CEA, CA199 and CA724, and the value as a prognostic indicator was also evaluated. The expression of MIC1 in ESCC cell lines, tissues were detected, and the inhibition of MIC1 antibody on ESCC was carried out in vitro and in vivo. The results showed that the serum MIC1 of ESCC was significantly higher than normal groups (P < 0.001), and was positively associated with tumor invasion (P = 0.030) as well as lymph node metastasis (P = 0.007). The sensitivity of MIC1 was significantly better than SCC, CEA, CA199 and CA724, especially for stage I ESCC. Patients with higher serum MIC1 also had a poorer prognosis in relapse-free (P = 0.050) and tumor-specific survival (P = 0.005). In vitro studies showed that the expression of MIC1 was upregulated in 37.5% (3/8) ESCC cell lines and 45% (18/40) tissues, and the transcription of MIC1 in tumor tissues was significantly higher than paired adjacent normal tissues (P = 0.001). The antibody of MIC1 inhibited the tumor growth (P < 0.001), and showing preference for tumor tissues in xenograft model. The decreased formation of neovascularization lumen may be involved in the mechanism. We conclude that MIC1 plays an important role in the progression of ESCC and can serve as a potential biomarker and therapeutic target for ESCC.
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