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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Reprogramming metastatic melanoma cells to assume a neural crest cell-like phenotype in an embryonic microenvironment
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Reprogramming metastatic melanoma cells to assume a neural crest cell-like phenotype in an embryonic microenvironment

机译：重编程转移性黑色素瘤细胞，使其在胚胎微环境中呈神经c细胞样表型

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摘要

Human metastatic melanoma cells express a dedifferentiated, plastic phenotype, which may serve as a selective advantage, because melanoma cells invade various microenvironments. Over the last three decades, there has been an increased focus on the role of the tumor microenvironment in cancer progression, with the goal of reversing the metastatic phenotype. Here, using an embryonic chick model, we explore the possibility of reverting the metastatic melanoma phenotype to its cell type of origin, the neural-crest-derived melanocyte. GFP-labeled adult human metastatic melanoma cells were transplanted in ovo adjacent to host chick premigratory neural crest cells and analyzed 48 and 96 h after egg reincubation. Interestingly, the transplanted melanoma cells do not form tumors. Instead, we find that transplanted melanoma cells invade surrounding chick tissues in a programmed manner, distributing along host neural-crest-cell migratory pathways. The invading melanoma cells display neural-crest-cell-like morphologies and populate host peripheral structures, including the branchial arches, dorsal root and sympathetic ganglia. Analysis of a melanocyte-specific phenotype marker (MART-1) and a neuronal marker (Tuj1) revealed a subpopulation of melanoma cells that invade the chick periphery and express MART-1 and Tuj1. Our results demonstrate the ability of adult human metastatic melanoma cells to respond to chick embryonic environmental cues, a subset of which may undergo a reprogramming of their metastatic phenotype. This model has the potential to provide insights into the regulation of tumor cell plasticity by an embryonic milieu, which may hold significant therapeutic promise.
机译：人类转移性黑色素瘤细胞表达去分化的可塑性表型，这可能是一种选择性优势，因为黑色素瘤细胞会侵袭各种微环境。在过去的三十年中，人们越来越关注肿瘤微环境在癌症进展中的作用，目的是逆转转移表型。在这里，我们使用胚胎小鸡模型，探讨将转移性黑色素瘤表型恢复为其起源的细胞类型，即神经neural衍生的黑色素细胞的可能性。 GFP标记的成年人类转移性黑色素瘤细胞被移植到卵中与宿主鸡移行前神经rest细胞相邻的卵中，并在卵重新孵育后48和96 h进行分析。有趣的是，移植的黑色素瘤细胞不会形成肿瘤。取而代之的是，我们发现移植的黑色素瘤细胞以编程方式侵入周围的鸡组织，沿着宿主神经neural细胞的迁移途径分布。侵袭性黑素瘤细胞表现出神经rest细胞样形态，并聚集宿主外周结构，包括branch弓，背根和交感神经节。黑色素细胞特异性表型标记（MART-1）和神经元标记（Tuj1）的分析显示，黑色素瘤细胞亚群侵入雏鸡外周并表达MART-1和Tuj1。我们的结果证明了成年人类转移性黑色素瘤细胞对雏鸡胚胎环境线索有反应的能力，其中一部分可能会经历对其转移表型的重新编程。该模型有可能提供有关胚胎环境对肿瘤细胞可塑性调节的见解，这可能具有重要的治疗前景。

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