Cell and Developmental Biology, Institute of Anatomy, University of Zurich, Winterthurerstrasse 190, 8057 Zürich, Switzerland.
Institute of Veterinary Biochemistry and Molecular Biology, University of Zurich, Winterthurerstrasse 190, 8057 Zürich, Switzerland.
Nat Commun. 2015 Jan 22;6:6051. doi: 10.1038/ncomms7051.
Increased activity of the epigenetic modifier EZH2 has been associated with different cancers. However, evidence for a functional role of EZH2 in tumorigenesis in vivo remains poor, in particular in metastasizing solid cancers. Here we reveal central roles of EZH2 in promoting growth and metastasis of cutaneous melanoma. In a melanoma mouse model, conditional Ezh2 ablation as much as treatment with the preclinical EZH2 inhibitor GSK503 stabilizes the disease through inhibition of growth and virtually abolishes metastases formation without affecting normal melanocyte biology. Comparably, in human melanoma cells, EZH2 inactivation impairs proliferation and invasiveness, accompanied by re-expression of tumour suppressors connected to increased patient survival. These EZH2 target genes suppress either melanoma growth or metastasis in vivo, revealing the dual function of EZH2 in promoting tumour progression. Thus, EZH2-mediated epigenetic repression is highly relevant especially during advanced melanoma progression, which makes EZH2 a promising target for novel melanoma therapies.
表观遗传修饰酶 EZH2 的活性增加与多种癌症有关。然而,EZH2 在体内肿瘤发生中的功能作用的证据仍然很少,特别是在转移性实体瘤中。在这里,我们揭示了 EZH2 在促进皮肤黑色素瘤生长和转移中的核心作用。在黑色素瘤小鼠模型中,条件性 Ezh2 缺失,以及使用临床前 EZH2 抑制剂 GSK503 治疗,通过抑制生长稳定疾病,并几乎消除转移形成,而不影响正常黑素细胞生物学。类似地,在人类黑色素瘤细胞中,EZH2 失活会损害增殖和侵袭性,同时重新表达与增加患者生存相关的肿瘤抑制因子。这些 EZH2 靶基因在体内抑制黑色素瘤的生长或转移,揭示了 EZH2 在促进肿瘤进展中的双重功能。因此,EZH2 介导的表观遗传抑制在晚期黑色素瘤进展中尤为重要,这使得 EZH2 成为新型黑色素瘤治疗的有前途的靶点。