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首页> 外文期刊>Lung cancer: Journal of the International Association for the Study of Lung Cancer >Interleukin-8 stimulates cell proliferation in non-small cell lung cancer through epidermal growth factor receptor transactivation.
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Interleukin-8 stimulates cell proliferation in non-small cell lung cancer through epidermal growth factor receptor transactivation.

机译：Interleukin-8刺激细胞增殖非小细胞肺癌表皮生长因子受体transactivation。

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摘要

Interleukin-8 (IL-8; CXCL8) is a cytokine of the CXC chemokine family that is involved in neutrophil recruitment and activation. In addition, IL-8 has been implicated in a wide variety of other processes, including angiogenesis and metastasis in lung cancer. Lung adenocarcinoma and muco-epidermoid carcinoma cells produce substantial amounts of IL-8, and express both CXCR1 and CXCR2 IL-8 receptors. We hypothesized that IL-8 stimulates proliferation of non-small cell lung cancer cells, involving transactivation of the epidermal growth factor receptor (EGFR). The EGFR plays a central role in regulating cell proliferation and it has been therefore implicated in lung cancer. Both EGFR ligands and transactivation of the receptor may lead to downstream signalling events, including mitogen-activated protein kinase (MAPK) activation. Transactivation of the EGFR has been shown to occur in response to ligands of various G-protein coupled receptors (GPCRs) and involves metalloproteinase-mediated release of membrane bound EGFR ligands. The aim of the present study was to investigate the effect of IL-8 on proliferation of lung adenocarcinoma and muco-epidermoid carcinoma cells, and to explore the mechanisms leading to this proliferation in two different non-small cell lung cancer cell lines (A549 and NCI-H292). In both NSCLC cell lines, we observed that IL-8 stimulates epithelial cell proliferation in a dose-dependent manner. The ability of IL-8 to increase cell proliferation was blocked both by an inhibitor of EGFR tyrosine kinase, by a specific anti-EGFR blocking antibody and by a panmetalloproteinase inhibitor. Similar results were obtained using the GPCR inhibitor pertussis toxin. Inhibition of the MAPK p42/44 (ERK1/2) also blocked the mitogenic effect of IL-8, while a p38 MAPK inhibitor did not affect IL-8-induced cell proliferation. These results suggest that IL-8 increases cell proliferation in NSCLC cell lines via transactivation of the EGFR and that this mechanism involves metalloproteinase activity.
机译：Interleukin-8(引发;科学家参与的趋化因子家族中性粒细胞招聘和激活。另外,引发涉及广泛各种各样的其他进程,包括在肺癌血管生成和转移。腺癌和muco-epidermoid癌细胞产生大量的引发,表达和CXCR1 CXCR2引发受体。假设引发刺激增殖非小细胞肺癌细胞,包括transactivation表皮生长因子受体(EGFR)。调节细胞增殖和它因此与肺癌。配体和受体的transactivation导致下游信号事件,包括增殖蛋白激酶(MAPK)激活。显示发生在应对不同的配体g蛋白耦合受体(GPCRs)和涉及metalloproteinase-mediated释放膜表皮生长因子受体配体。是研究引发的影响肺腺癌和扩散muco-epidermoid癌细胞,探索导致这种扩散的机制两个不同的非小细胞肺癌细胞(A549和NCI-H292行)。行,我们观察到引发刺激上皮细胞增殖存在剂量依赖的相关性的方式。扩散受阻的抑制剂表皮生长因子受体酪氨酸激酶,通过特定的anti-EGFR抑制性抗体和panmetalloproteinase抑制剂。GPCR抑制剂百日咳毒素。的MAPK p42/44 (ERK1/2)也封锁了引发的促有丝分裂的影响,而p38 MAPK抑制剂并不影响IL-8-induced细胞扩散。增加在非小细胞肺癌细胞株细胞增殖通过transactivation表皮生长因子受体,这机制包括金属蛋白酶活性。

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