YES驱动的转移性和增殖性肝细胞癌的合成小鼠模型。

IF 4 3区 医学 Q2 CELL BIOLOGY
Disease Models & Mechanisms Pub Date : 2024-07-01 Epub Date: 2024-07-25 DOI:10.1242/dmm.050553
Laure Voisin, Marjorie Lapouge, Marc K Saba-El-Leil, Melania Gombos, Joaquim Javary, Vincent Q Trinh, Sylvain Meloche
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引用次数: 0

摘要

肝细胞癌(HCC)是一种尚未满足大量医疗需求的疾病,已成为一个全球性的健康问题。由于对 HCC 发病机制的不完全了解以及相关临床前动物模型数量有限,HCC 靶向疗法的开发一直受到阻碍。我们最近发现了一种以前未曾描述过的 YES 激酶(由 YES1 编码)依赖于 HCC 的致癌信号通路。为了模拟这一 HCC 亚群,我们从表达活化人 YES 的转基因小鼠的肝脏肿瘤中建立了一系列合成细胞系。这些细胞系(称为 HepYF)富含干细胞和祖细胞标志物,增殖迅速,具有高 SRC 家族激酶(SFK)活性和激活的有丝分裂信号通路的特征。转录组分析表明,HepYF 细胞是最具侵袭性的增殖类 G3 亚群的代表。HepYF 细胞正位移植到合成宿主体内后会形成快速生长的转移性肿瘤。索拉非尼或 SFK 抑制剂达沙替尼可明显抑制 HepYF 肿瘤的生长。新的HepYF HCC细胞系为研究HCC的发病机制以及测试新型小分子抑制剂和免疫疗法提供了相关的临床前模型。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Syngeneic mouse model of YES-driven metastatic and proliferative hepatocellular carcinoma.

Hepatocellular carcinoma (HCC) is a disease of high unmet medical need that has become a global health problem. The development of targeted therapies for HCC has been hindered by the incomplete understanding of HCC pathogenesis and the limited number of relevant preclinical animal models. We recently unveiled a previously uncharacterized YES kinase (encoded by YES1)-dependent oncogenic signaling pathway in HCC. To model this subset of HCC, we established a series of syngeneic cell lines from liver tumors of transgenic mice expressing activated human YES. The resulting cell lines (referred to as HepYF) were enriched for expression of stem cell and progenitor markers, proliferated rapidly, and were characterized by high SRC family kinase (SFK) activity and activated mitogenic signaling pathways. Transcriptomic analysis indicated that HepYF cells are representative of the most aggressive proliferation class G3 subgroup of HCC. HepYF cells formed rapidly growing metastatic tumors upon orthotopic implantation into syngeneic hosts. Treatment with sorafenib or the SFK inhibitor dasatinib markedly inhibited the growth of HepYF tumors. The new HepYF HCC cell lines provide relevant preclinical models to study the pathogenesis of HCC and test novel small-molecule inhibitor and immunotherapy approaches.

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来源期刊
Disease Models & Mechanisms
Disease Models & Mechanisms 医学-病理学
CiteScore
6.60
自引率
7.00%
发文量
203
审稿时长
6-12 weeks
期刊介绍: Disease Models & Mechanisms (DMM) is an online Open Access journal focusing on the use of model systems to better understand, diagnose and treat human disease.
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