Department of Medicine.
Department of Molecular and Medical Pharmacology, and.
J Clin Invest. 2021 Jun 15;131(12). doi: 10.1172/JCI145859.
Melanoma dedifferentiation has been reported to be a state of cellular resistance to targeted therapies and immunotherapies as cancer cells revert to a more primitive cellular phenotype. Here, we show that, counterintuitively, the biopsies of patient tumors that responded to anti-programmed cell death 1 (anti-PD-1) therapy had decreased expression of melanocytic markers and increased neural crest markers, suggesting treatment-induced dedifferentiation. When modeling the effects in vitro, we documented that melanoma cell lines that were originally differentiated underwent a process of neural crest dedifferentiation when continuously exposed to IFN-γ, through global chromatin landscape changes that led to enrichment in specific hyperaccessible chromatin regions. The IFN-γ-induced dedifferentiation signature corresponded with improved outcomes in patients with melanoma, challenging the notion that neural crest dedifferentiation is entirely an adverse phenotype.
黑色素瘤去分化已被报道为细胞对靶向治疗和免疫治疗产生抵抗的状态,因为癌细胞恢复到更原始的细胞表型。在这里,我们表明,与直觉相反,对抗程序性细胞死亡 1(抗 PD-1)治疗有反应的患者肿瘤活检显示黑色素细胞标记物表达降低,神经嵴标记物增加,提示治疗诱导的去分化。当在体外模拟这些影响时,我们记录到最初分化的黑色素瘤细胞系在持续暴露于 IFN-γ时经历了神经嵴去分化的过程,通过导致特定高可及染色质区域富集的全染色质景观变化。IFN-γ诱导的去分化特征与黑色素瘤患者的更好结局相对应,这挑战了神经嵴去分化完全是一种不良表型的观点。