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血管生成因子白细胞介素8在非小细胞肺癌/肺成纤维细胞共培养物中被诱导产生。

The angiogenic factor interleukin 8 is induced in non-small cell lung cancer/pulmonary fibroblast cocultures.

作者信息

Anderson I C, Mari S E, Broderick R J, Mari B P, Shipp M A

机构信息

Department of Adult Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA.

出版信息

Cancer Res. 2000 Jan 15;60(2):269-72.

Abstract

The interactions between tumor cells and surrounding stromal elements may promote the release of angiogenic factors. Although interleukin 8 (IL-8) is a major angiogenic factor in non-small cell lung cancer (NSCLC), the stromal contribution to IL-8 expression in primary NSCLC remains to be defined. To elucidate the role of stromal elements in NSCLC IL-8 production, normal pulmonary fibroblasts were cocultured with six representative NSCLC lines in direct and transwell assays. IL-8 transcripts and protein were consistently induced in fibroblasts and a subset of NSCLCs as a consequence of tumor/stromal coculture. In these cocultures, IL-8 was induced by IL-1alpha and an additional, as yet unidentified, soluble factor. These data underscore the importance of tumor/stromal interaction in the production of angiogenic peptides such as IL-8 in NSCLC.

摘要

肿瘤细胞与周围基质成分之间的相互作用可能促进血管生成因子的释放。尽管白细胞介素8(IL-8)是非小细胞肺癌(NSCLC)中的主要血管生成因子,但基质对原发性NSCLC中IL-8表达的作用仍有待确定。为了阐明基质成分在NSCLC产生IL-8中的作用,在直接共培养和Transwell实验中将正常肺成纤维细胞与六种代表性NSCLC细胞系进行共培养。肿瘤/基质共培养的结果是,成纤维细胞和一部分NSCLC细胞中IL-8转录本和蛋白持续被诱导产生。在这些共培养体系中,IL-1α和另一种尚未鉴定的可溶性因子可诱导IL-8产生。这些数据强调了肿瘤/基质相互作用在NSCLC中产生血管生成肽(如IL-8)中的重要性。

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