ELR+ CXC chemokine expression in benign and malignant colorectal conditions.
ELR+ CXC chemokine expression in benign and malignant colorectal conditions.
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DOI：
10.1186/1471-2407-8-178
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发表时间：
2008-06-25
期刊：
影响因子：
3.8
通讯作者：
Schilling MK
中科院分区：
文献类型：
--
作者：
Rubie C;Frick VO;Wagner M;Schuld J;Gräber S;Brittner B;Bohle RM;Schilling MK
CXCR 2趋化因子配体CXCL 1、CXCL 5和CXCL 6被证明参与化学吸引、炎症反应、肿瘤生长和血管生成。在这里，我们比较分析了它们在结直肠腺瘤（CRA）（n = 30）以及结直肠癌（CRC）（n = 48）和相应的结直肠肝转移（CRLM）（n = 16）患者的切除标本中的表达谱。通过显微切割、实时定量PCR（Q-RT-PCR）、酶联免疫吸附试验（ELISA）和免疫组织化学（IHC）评估趋化因子的表达。与CXCL 6相反，我们证明了CXCL 1和CXCL 5 mRNA和蛋白表达在CRC和CRLM组织标本中相对于其匹配的肿瘤相邻组织显著上调。此外，证明两种趋化因子配体在CRC组织中的表达显著高于CRA组织，从而表明从癌前状态向恶性状态发展的转变的进行性增加。尽管CRC患者中CXCL 1/CXCL 5蛋白表达谱的比较分析显示，CXCL 1的绝对表达水平显著高于CXCL 5，但CRC和CRLM组织中CXCL 5的mRNA和蛋白过表达要显著得多与CXCL 1（在CRC组织中分别为5倍和3.5倍）相比，CXCL 1在CRC组织中分别为80倍和60倍。我们的研究结果表明CXCL 1和CXCL 5表达与CRC和CRLM之间存在显著相关性，这表明两种趋化因子配体在从CRA进展为CRC中具有潜在作用，因此，在CRC的起始中具有潜在作用。
CXCR2 chemokine ligands CXCL1, CXCL5 and CXCL6 were shown to be involved in chemoattraction, inflammatory responses, tumor growth and angiogenesis. Here, we comparatively analyzed their expression profile in resection specimens from patients with colorectal adenoma (CRA) (n = 30) as well as colorectal carcinoma (CRC) (n = 48) and corresponding colorectal liver metastases (CRLM) (n = 16). Chemokine expression was assessed by microdissection, quantitative real-time PCR (Q-RT-PCR), the enzyme-linked immunosorbent assay (ELISA) and immunohistochemistry (IHC). In contrast to CXCL6, we demonstrated CXCL1 and CXCL5 mRNA and protein expression to be significantly up-regulated in CRC and CRLM tissue specimens in relation to their matched tumor neighbor tissues. Moreover, both chemokine ligands were demonstrated to be significantly higher expressed in CRC tissues than in CRA tissues thus indicating a progressive increase in the transition from the premalignant condition to the development of the malignant status. Although a comparative analysis of the CXCL1/CXCL5 protein expression profiles in CRC patients revealed that the absolute expression level of CXCL1 was significantly higher in comparison to CXCL5, mRNA- and protein overexpression of CXCL5 in CRC and CRLM tissues was much more pronounced (80- and 60- fold in CRC tissues, respectively) in comparison to CXCL1 (5- and 3.5- fold in CRC tissues, respectively). Our results demonstrate a significant association between CXCL1 and CXCL5 expression with CRC and CRLM suggesting for both chemokine ligands a potential role in the progression from CRA to CRC and thus, in the initiation of CRC.
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