Reduced expression of the CXCR4 receptor mRNA in hepatocellular carcinoma and lack of inducibility of its ligand alpha-chemokine hIRH/SDF1alpha/PBSF in vitro.
Reduced expression of the CXCR4 receptor mRNA in hepatocellular carcinoma and lack of inducibility of its ligand alpha-chemokine hIRH/SDF1alpha/PBSF in vitro.
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DOI：
10.3892/ijo.14.5.927
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发表时间：
1999-05
影响因子：
5.2
通讯作者：
N. Begum;K. Shibuta;M. Mori;G. Barnard
中科院分区：
文献类型：
--
作者：
N. Begum;K. Shibuta;M. Mori;G. Barnard
肝细胞癌和邻近非恶性组织之间的差异cDNA显示先前检测到PCR产物hIRH（肝细胞瘤中的人内分泌减少），相当于SDF 1 α/PBSF，其mRNA从人肝细胞癌和其他恶性和癌前样品和恶性细胞系中丢失。目前还没有关于hIRH/SDF 1 α/PBSF受体CXCR 4在恶性组织中的mRNA表达情况的报道。我们在这里报告，有一个减少CXCR 4的mRNA表达在肝细胞癌的估计由北方印迹和RT-PCR，并与相邻的非恶性组织相比。平均（平均SD）肿瘤/正常比CXCR 4 mRNA的表达，通过RT-PCR测定，为0.65 - 0.36在10对肝细胞癌。在一系列恶性肿瘤细胞系中，CXCR 4 mRNA表达没有一致的丢失。hIRH的3 ′-非编码区具有典型的早期反应基因元件序列。尽管存在这些3 ′-元件，但在诱导同源物CXC内分泌IL-8表达的条件下，肿瘤坏死因子α、白细胞介素-2、脂多糖或佛波醇肉豆蔻乙酸酯在人肺癌A549细胞中没有诱导hIRH基因表达，紫外线照射在人黑色素瘤细胞系SB-2中也没有诱导hIRH基因表达。此外，有没有诱导hIRH基因表达，而是抑制后，血清或细胞因子添加到血清剥夺成纤维细胞系，在体外小鼠骨髓制备，和单核细胞系THP-1。
Differential cDNA displays between hepatocellular carcinoma and adjacent non-malignant tissues have previously detected a PCR product, hIRH (human intercrine reduced in hepatomas), equivalent to SDF1alpha/PBSF whose mRNA was lost from human hepatocellular carcinoma and other malignant and pre-malignant samples and malignant cell lines. There are no reports to date of the mRNA status of the receptor for hIRH/SDF1alpha/PBSF, CXCR4 in malignant tissues. We report here that there is a reduction in the mRNA expression of CXCR4 in hepatocellular carcinoma as estimated by Northern blot and RT-PCR and compared to the adjacent non-malignant tissue. The average (mean SD) tumor/normal ratio for CXCR4 mRNA expression, determined by RT-PCR, was 0.65 0.36 in 10 pairs of hepatocellular carcinomas. There was no consistent loss of CXCR4 mRNA expression in a range of malignant cell lines. The 3'-non-coding region of hIRH, had typical early response gene element sequences. Despite the presence of these 3'-elements there was no induction of hIRH gene expression in human lung carcinoma A549 cells by tumor necrosis factor alpha, interleukin-2, lipopolysaccharide or phorbol myristic acetate, nor in human melanoma cell line SB-2 by uv irradiation, under conditions which induced the homologue CXC intercrine IL-8 expression. Furthermore, there was no induction of hIRH gene expression, but rather a suppression, upon serum or cytokine addition to serum-deprived fibroblast cell lines, to an in vitro mouse bone marrow preparation, and to monocytic cell line THP-1.