Restored Ketosis Drives Anticancer Immunity in Colorectal Cancer.
Restored Ketosis Drives Anticancer Immunity in Colorectal Cancer.
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恢复酮症驱动结直肠癌的抗癌免疫。
DOI：
10.1158/0008-5472.can-22-0686
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发表时间：
2022-04-15
期刊：
影响因子：
11.2
通讯作者：
中科院分区：
文献类型：
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作者：
饮食干预（包括改变特定常量营养素的数量或类型）已被证明可以在临床前肿瘤模型中介导抗肿瘤作用，但其潜在机制仅部分了解。在本期《癌症研究》中，Wei 及其同事证明，恢复结直肠癌微环境中的生酮作用会减少癌症相关成纤维细胞依赖 KLF5 的 CXCL12 合成，最终增强免疫效应细胞对肿瘤的浸润，并提高 PD-1 特异性免疫检查点抑制剂的治疗效果。这些发现为结直肠癌微环境中生酮抑制和免疫逃避之间提供了一种新颖的、治疗上可行的联系。
Dietary interventions including alterations in the amount or type of specific macronutrients have been shown to mediate antineoplastic effects in preclinical tumor models, but the underlying mechanisms are only partially understood. In this issue of Cancer Research, Wei and colleagues demonstrate that restoring ketogenesis in the colorectal cancer microenvironment decreases the KLF5-dependent synthesis of CXCL12 by cancer-associated fibroblasts, ultimately enhancing tumor infiltration by immune effector cells and increasing the therapeutic efficacy of an immune checkpoint inhibitor specific for PD-1. These findings provide a novel, therapeutically actionable link between suppressed ketogenesis and immunoevasion in the colorectal cancer microenvironment.