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SR 11302,一种AP - 1抑制剂,可减少体外4D肺癌模型中转移病灶的形成。

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

作者信息

Mishra Dhruva Kumar, Kim Min P

机构信息

Department of Surgery, Houston Methodist Research Institute, 6670 Bertner Ave, Houston, TX, 77030, USA.

Department of Surgery, Weill Cornell Medical College, Houston Methodist Hospital, Houston, TX, 77030, USA.

出版信息

Cancer Microenviron. 2017 Dec;10(1-3):95-103. doi: 10.1007/s12307-017-0202-0. Epub 2017 Nov 24.

Abstract

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.

摘要

激活蛋白(AP)-1是一种转录因子,在细胞分化、增殖和凋亡中发挥重要作用。对在离体4D肺癌模型上生长的肿瘤细胞进行分析发现,与原发性肿瘤相比,循环肿瘤细胞(CTC)中AP-1、c-Fos和c-Jun的成分有所增加。我们的目的是确定AP-1抑制剂SR11302是否能减少4D模型中转移病灶的形成。将人肺癌细胞系A549、H1299和H460在4D模型中培养,并用SR11302(1μM)处理。我们比较了SR11302处理后转移部位的细胞数量以及从4D模型中分离出的活CTC数量与在培养皿中经SR11302处理/未处理的亲代细胞数量。在用SR11302处理的接种了H460(p = 0.009)、A549(p = 0.01)或H1299(p = 0.02)细胞的4D模型中,转移部位每高倍视野的肿瘤细胞明显减少。此外,接种了H460(p = 0.04)、A549(p = 0.008)或H1299(p = 0.01)细胞的经SR11302处理的4D模型中的CTC在培养4天后,活肿瘤细胞数量明显少于各自未处理的对照。然而,SR11302对在培养皿(2D)上生长的亲代H460(p = 0.87)、A549(p = 0.93)或H1299(p = 0.25)细胞的活力没有影响。由于三种细胞系中存在独立但共同的途径,SR11302可减少离体4D肺癌模型中转移病灶的形成。离体4D模型可能为更好地理解转移的复杂过程提供一种工具。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3995/5750205/ea3e8ad57b60/12307_2017_202_Fig1_HTML.jpg

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