AP-1抑制剂SR 11302在体外4D肺癌模型中减少转移灶形成

Q2 Medicine Cancer Microenvironment Pub Date : 2017-12-01 Epub Date: 2017-11-24 DOI:10.1007/s12307-017-0202-0
Dhruva Kumar Mishra, Min P Kim
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引用次数: 15

摘要

激活蛋白(Activator protein, AP) -1是一种转录因子,在细胞分化、增殖和凋亡过程中起重要作用。体外4D肺癌模型肿瘤细胞分析显示,循环肿瘤细胞(CTC)中AP-1、c-Fos和c-Jun成分较原发肿瘤增加。我们的目的是在4D模型中确定AP-1抑制剂SR11302是否能减少转移灶的形成。在4D模型中培养人肺癌细胞株A549、H1299和H460,并用SR11302 (1 μM)处理。我们比较了SR11302处理后转移部位的细胞数量,以及在培养皿中从4D模型中分离出的与SR11302处理/未处理的亲本细胞的存活ctc数量。SR11302处理的H460 (p = 0.009)、A549 (p = 0.01)和H1299 (p = 0.02)细胞在4D模型转移部位的高倍视野肿瘤细胞数量显著减少。此外,SR11302处理4D模型的CTCs,接种H460 (p = 0.04), A549 (p = 0.008)或H1299 (p = 0.01)细胞,在培养4天后,存活的肿瘤细胞明显少于未处理的对照组。然而,SR11302对在培养皿上生长的亲本H460 (p = 0.87)、A549 (p = 0.93)和H1299 (p = 0.25)细胞的存活率没有影响(2D)。SR11302在体外4D肺癌模型中减少了转移灶的形成,这是由于三个细胞系之间存在一个独立而共同的通路。体外4D模型可以为更好地了解复杂的转移过程提供工具。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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SR 11302, an AP-1 Inhibitor, Reduces Metastatic Lesion Formation in Ex Vivo 4D Lung Cancer Model.

Activator protein (AP) -1 is a transcription factor, plays important role in cell differentiation, proliferation and apoptosis. Analysis of tumor cells grown on ex vivo 4D lung cancer model shows increase in components of AP-1, c-Fos and c-Jun in circulating tumor cells (CTC) compared to primary tumor. Our aim was to determine whether the AP-1 inhibitor SR11302 reduces metastatic lesion formation in the 4D model. Human lung cancer cell lines A549, H1299, and H460 were grown in the 4D model and treated with SR11302 (1 μM). We compared the number of cells in the metastatic site upon SR11302 treatment and number of viable CTCs isolated from the 4D model with parental cells treated/untreated with SR11302 on a petri dish. There were significantly fewer tumor cells per high-power field on metastatic site in 4D model seeded with H460 (p = 0.009), A549 (p = 0.01), or H1299 (p = 0.02) cells treated with SR11302. Furthermore, the CTCs from SR11302 treated 4D models, seeded with H460 (p = 0.04), A549 (p = 0.008), or H1299 (p = 0.01) cells had significantly fewer viable tumor cells after 4 days in culture than the respective untreated control. However, the SR11302 had no impact on the viability of parental H460 (p = 0.87), A549 (p = 0.93), or H1299 (p = 0.25) cells grown on a petri dish (2D). SR11302 reduces metastatic lesion formation in the ex vivo 4D lung cancer model due to the presence of an independent yet common pathway among three cell lines. The ex vivo 4D model may provide a tool to better understand the complex process of metastasis.

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来源期刊
Cancer Microenvironment
Cancer Microenvironment Medicine-Oncology
CiteScore
4.90
自引率
0.00%
发文量
0
期刊介绍: Cancer Microenvironment is the official journal of the International Cancer Microenvironment Society (ICMS). It publishes original studies in all aspects of basic, clinical and translational research devoted to the study of cancer microenvironment. It also features reports on clinical trials. Coverage in Cancer Microenvironment includes: regulation of gene expression in the cancer microenvironment; innate and adaptive immunity in the cancer microenvironment, inflammation and cancer; tumor-associated stroma and extracellular matrix, tumor-endothelium interactions (angiogenesis, extravasation), cancer stem cells, the metastatic niche, targeting the tumor microenvironment: preclinical and clinical trials.
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