STTT:北京协和医院团队发现烟草致癌物如何诱导代谢和免疫抑制

2022-09-12 转化医学网 网络

IDO1-高吸烟者患者可能受益于含有针对PD1 / PD-L1和IDO1抑制剂的抗体的组合方案。临床试验建议测试IDO1抑制剂和PD1 / PD-L1阻断的组合疗法在治疗高水平IDO1的吸烟患者中的有效性。

IDO1是分解代谢色氨酸(Trp)以促进调节性T细胞并抑制CD8 T细胞的酶,由几种内在信号通路调节。研究发现烟草烟雾是一个主要的公共卫生问题,每年导致全球800万人死亡,它在体外和体内诱导正常和恶性肺上皮细胞中的IDO1。致癌尼古丁衍生的亚硝胺酮是通过激活转录因子c-Jun上调IDO1的烟草化合物,其具有IDO1启动子的结合位点。临床上,非小细胞肺癌吸烟患者表现出高IDO1水平和低色氨酸比值。在非小细胞肺癌患者中,IDO1较低的吸烟者对抗PD1抗体治疗的反应优于IDO1较高的吸烟者。

该研究发布于《Signal Transduction and Targeted Therapy》,表明烟草烟雾诱导IDO1分解代谢色氨酸和免疫抑制以促进致癌,较低的IDO1可能是吸烟者抗PD1抗体的潜在生物标志物,而IDO1高吸烟者患者可能受益于IDO1抑制剂与抗PD1抗体的组合。

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https://www.nature.com/articles/s41392-022-01127-3

头号危险因素——肺癌

肺癌是癌症相关死亡的最常见原因,全世界每年有2,206,771例新病例和1,796,144例死亡。这种疾病包括小细胞肺癌和非小细胞肺癌,肺鳞状细胞癌和大细胞肺癌。烟草烟雾是肺癌的头号危险因素,在肺癌死亡人数中占比大于80%。烟草烟雾通过诱导基因组突变对暴露的人群产生有害影响,表观遗传异常,慢性癌症促进性炎症和免疫逃逸促进肺癌。然而,介导烟草烟雾诱导的肺癌发生的关键分子仍有待鉴定,烟草对细胞代谢的影响仍然很大程度上是未知的。

色氨酸与IDO1

色氨酸是一种不可或缺的氨基酸,主要从饮食中获得,真核细胞使用它来合成蛋白质和神经递质/神经调节剂,并产生包括犬尿氨酸在内的几种代谢物。IDO1是一种含胞质血红素的酶,其功能是催化色氨酸降解。

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IDO1一直被认为是一个有吸引力的药物靶点,几种组合疗法,包括IDO1抑制剂与抗PD1抗体(如培布利珠单抗)联合使用已被提议。不幸的是,在一项III期试验中,联合使用依帕多司他和佩姆单抗并没有改善黑色素瘤患者的无进展生存期。这些观察结果表明,患者分层对于基于IDO1抑制剂的治疗非常重要,阐明IDO1与其他途径之间的串扰以及癌症中IDO1组成性激活的潜在机制对于制定有效的治疗策略至关重要。

Trp / Kyn比率

在这项新研究中,北京协和医院团队测试了色氨酸(Trp)和犬尿氨酸(Kyn)的血浆浓度,比较了吸烟和非吸烟者非小细胞肺癌患者的Trp / Kyn比率,分析了香烟烟雾提取物(CSE)和相关致癌物质对IDO1表达的影响,并研究了其潜在机制。研究发现烟草烟雾及其致癌物诱导Trp / Kyn失衡和CD8 T细胞抑制。

研究表明烟草烟雾可以通过亚硝胺酮诱导的IDO1上调来增强人肺上皮细胞和小鼠中的色氨酸代谢。在非小细胞肺癌患者中观察到细胞和动物模型的结果,吸烟患者的IDO1表达水平较高,Trp / Kyn比率低于非吸烟患者。这些结果表明,NSCLC中异常的Trp代谢可能是烟草暴露的结果,癌症中其他代谢功能障碍的原因值得进一步研究。然而,72名吸烟患者中有26名(36.1%)的Trp/ Kyn比率很高,这可能是由于他们对烟草致癌物的代谢活性和他们吸烟的烟草成分的差异。此外,亚硝胺酮对IDO1的上调为肺癌中环境基因相互作用提供了一个新的例子。

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结果还表明,IDO1-高吸烟者患者可能受益于含有针对PD1 / PD-L1和IDO1抑制剂的抗体的组合方案。临床试验建议测试IDO1抑制剂和PD1 / PD-L1阻断的组合疗法在治疗高水平IDO1的吸烟患者中的有效性。

参考资料:

https://www.nature.com/articles/s41392-022-01127-3

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    2022-09-13 mnda
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    2022-09-13 jambiya
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    2022-09-13 qjddjq
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