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肿瘤来源的EZH2功能获得性突变引起的表观遗传重编程促进侵袭性三维细胞形态并增强黑色素瘤肿瘤生长。

Epigenetic reprogramming by tumor-derived EZH2 gain-of-function mutations promotes aggressive 3D cell morphologies and enhances melanoma tumor growth.

作者信息

Barsotti Anthony M, Ryskin Michael, Zhong Wenyan, Zhang Wei-Guo, Giannakou Andreas, Loreth Christine, Diesl Veronica, Follettie Maximillian, Golas Jonathon, Lee Michelle, Nichols Timothy, Fan Conglin, Li Gang, Dann Stephen, Fantin Valeria R, Arndt Kim, Verhelle Dominique, Rollins Robert A

机构信息

Oncology Research Unit, Pfizer Worldwide Research and Development, Pearl River, NY 10965, USA.

Oncology Research Unit, Pfizer Worldwide Research and Development, Cambridge, MA 02140, USA.

出版信息

Oncotarget. 2015 Feb 20;6(5):2928-38. doi: 10.18632/oncotarget.2758.

Abstract

In addition to genetic alterations, cancer cells are characterized by myriad epigenetic changes. EZH2 is a histone methyltransferase that is over-expressed and mutated in cancer. The EZH2 gain-of-function (GOF) mutations first identified in lymphomas have recently been reported in melanoma (~2%) but remain uncharacterized. We expressed multiple EZH2 GOF mutations in the A375 metastatic skin melanoma cell line and observed both increased H3K27me3 and dramatic changes in 3D culture morphology. In these cells, prominent morphological changes were accompanied by a decrease in cell contractility and an increase in collective cell migration. At the molecular level, we observed significant alteration of the axonal guidance pathway, a pathway intricately involved in the regulation of cell shape and motility. Furthermore, the aggressive 3D morphology of EZH2 GOF-expressing melanoma cells (both endogenous and ectopic) was attenuated by EZH2 catalytic inhibition. Finally, A375 cells expressing exogenous EZH2 GOF mutants formed larger tumors than control cells in mouse xenograft studies. This study not only demonstrates the first functional characterization of EZH2 GOF mutants in non-hematopoietic cells, but also provides a rationale for EZH2 catalytic inhibition in melanoma.

摘要

除了基因改变外,癌细胞还具有众多表观遗传变化的特征。EZH2是一种组蛋白甲基转移酶,在癌症中过度表达且发生突变。最初在淋巴瘤中发现的EZH2功能获得性(GOF)突变最近在黑色素瘤中也有报道(约2%),但仍未得到充分表征。我们在A375转移性皮肤黑色素瘤细胞系中表达了多种EZH2 GOF突变,并观察到H3K27me3增加以及3D培养形态发生显著变化。在这些细胞中,显著的形态变化伴随着细胞收缩力的降低和集体细胞迁移的增加。在分子水平上,我们观察到轴突导向通路发生了显著改变,该通路与细胞形状和运动性的调节密切相关。此外,EZH2催化抑制减弱了表达EZH2 GOF的黑色素瘤细胞(内源性和异位性)的侵袭性3D形态。最后,在小鼠异种移植研究中,表达外源性EZH2 GOF突变体的A375细胞比对照细胞形成了更大的肿瘤。这项研究不仅首次展示了EZH2 GOF突变体在非造血细胞中的功能特征,还为黑色素瘤中EZH2催化抑制提供了理论依据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7292/4413628/6903929a2c97/oncotarget-06-2928-g001.jpg

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