本文显示肿瘤细胞破坏了CD8+T细胞中的甲硫氨酸代谢,从而降低了甲硫氨酸和SAM的细胞内水平,并导致组蛋白H3赖氨酸79二甲基化的缺失(H3K79me2),进而导致STAT5的低表达和T细胞免疫受损。从机制上讲,肿瘤细胞通过表达高水平的甲硫氨酸转运蛋白SLC43A2来过度地消耗甲硫氨酸,而竞争性地使T细胞无法获得甲硫氨酸。本文确定...
近日，发表在《Nature》上的一篇标题为：“Cancer SLC43A2 alters T cell methionine metabolism and histone methylation”的文章，证实了肿瘤细胞可通过高表达SLC43A2受体竞争抑制CD8+T细胞的甲硫氨酸代谢，干扰T细胞的肿瘤免疫。这提示我们，抑制肿瘤细胞的甲硫氨酸受体可潜在作为治疗肿瘤的新思路。在这篇文章中，研究...
Nature volume 585, pages 277–282 (2020)Cite this article 50k Accesses 159 Altmetric Metrics details Abstract Abnormal epigenetic patterns correlate with effector T cell malfunction in tumours1,2,3,4, but the cause of this link is unknown. Here we show that tumour cells disrupt methionine metabo...
近日,发表在《Nature》上的一篇标题为:“Cancer SLC43A2 alters T cell methionine metabolism and histone methylation”的文章,证实了肿瘤细胞可通过高表达SLC43A2受体竞争抑制CD8+T细胞的甲硫氨酸代谢,干扰T细胞的肿瘤免疫。这提示我们,抑制肿瘤细胞的甲硫氨酸受体可潜在作为治疗肿瘤的新思路。 在这篇文章中,研究人员...
Cancer SLC43A2 alters T cell methionine metabolism and histone methylation Yingjie Bian,Wei Li,[…]Weiping Zou Nature 2020 CD8+T cells mediate anti-tumour immunity. Unfortunately, tumor-infiltrating CD8+T cells are often dysfunctional (this is known as Tcell exhaustion). Abnormal epigenetic pattern...
Wei-Fen Xiehttps://ror.org/04tavpn47grid.73113.370000 0004 0369 1660Department of Gastroenterology, Changzheng HospitalNaval Medical University Shanghai ChinaNature Publishing Group UKNature Communications
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