558-ATF6α激活驱动肝癌发生与免疫抑制研究

这项研究揭示了ATF6α（一种内质网应激传感器）在肝细胞癌（HCC）中的关键致病作用。研究发现，肝细胞中ATF6α的持续激活通过抑制FBP1基因引发代谢重编程，导致糖原耗尽、乳酸堆积和肿瘤微环境的恶化。这种代谢变化通过诱导CD8+ T细胞竭制，形成了一个免疫抑制环境，从而加速癌症进展。然而，ATF6α的高表达也使肿瘤对免疫检查点阻断（ICB）疗法更加敏感。实验证明，利用反义寡核苷酸（ASOs）靶向抑制ATF6α，或结合抗PD-1治疗，能有效减轻肿瘤负担并提高生存率。这些发现为治疗肝癌提供了全新的代谢与免疫联合干预策略。References:* Li X, Lebeaupin C, Kadianaki A, et al. Activated ATF6α is a hepatic tumour driver restricting immunosurveillance[J]. Nature...去小宇宙查看完整单集简介前往小宇宙评论区与主播互动

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这项研究揭示了ATF6α（一种内质网应激传感器）在肝细胞癌（HCC）中的关键致病作用。研究发现，肝细胞中ATF6α的持续激活通过抑制FBP1基因引发代谢重编程，导致糖原耗尽、乳酸堆积和肿瘤微环境的恶化。这种代谢变化通过诱导CD8+...

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