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首页> 外文期刊>Cytokine >Down-regulation of CXCL1 inhibits tumor growth in colorectal liver metastasis
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Down-regulation of CXCL1 inhibits tumor growth in colorectal liver metastasis

机译：CXCL1的下调抑制大肠肝转移中肿瘤的生长

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As part of ongoing studies to obtain a global picture of invasion related events in colorectal liver metastases, here, we report our findings on gene expression of the pro-angiogenic subgroup of chemokines, the CXCL-ELR+ chemokines. Apart from their pro-angiogenic and chemoattractant function, these chemokines appear to also contribute to tumor cell transformation, growth and invasion. In our nude mouse model of colorectal liver metastases, we found CXCL1,2,3,5 and 8 (IL-8) to be up-regulated in the tumor cells of the invasion front as compared to the tumor cells in the inner parts of the tumor. ShRNA mediated down-regulation of the most prominently up-regulated group member, CXCL1/gro-alpha resulted in inhibition of cell viability, invasion and proliferation. In vivo, down-regulation of CXCL1 resulted in a nearly complete prevention of tumor growth in nude mice. Mechanistically, auto-regulatory mechanisms involving NF-kappaB and Akt appear to be involved in pro-tumorigenic functions of CXCL1.
机译：作为获得大肠肝转移中侵袭相关事件的全球图片的正在进行的研究的一部分，在这里，我们报告对促血管生成因子趋化因子CXCL-ELR +趋化因子亚组基因表达的发现。除了其促血管生成和化学吸引功能外，这些趋化因子似乎还有助于肿瘤细胞的转化，生长和侵袭。在我们的结肠直肠癌肝转移裸鼠模型中，我们发现与侵袭前线的肿瘤细胞相比，CXCL1、2、3、5和8（IL-8）在侵袭前沿的肿瘤细胞中被上调。肿瘤。 ShRNA介导的最显着上调的组成员CXCL1 / gro-alpha的下调导致细胞活力，侵袭和增殖的抑制。在体内，CXCL1的下调导致裸鼠几乎完全防止肿瘤生长。从机制上讲，涉及NF-κB和Akt的自动调节机制似乎与CXCL1的促肿瘤发生功能有关。

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