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在MiT/TFE转位细胞癌中,mTOR介导的B7-H3的上调

Huili Li¹, Adrianna Amaral¹, Thiago Vidotto¹

¹Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.

The Journal of pathology

|November 3, 2025

概括

由于mTOR信号激活,B7-H3 (CD276) 在MiT/TFE重排的转位细胞癌 (tRCC) 中被上调. 这表明B7-H3是攻击性tRCC的潜在治疗点,特别是在转移性病例中.

科学领域:

在瘤学瘤学.
免疫学免疫学免疫学
分子生物学分子生物学

背景情况:

B7-H3 (CD276) 是一种有前途的免疫调节标,用于各种癌症.
MiT/TFE重排的转位细胞癌 (tRCC) 具有侵略性,免疫力低下,并表现出高mTOR活性.

研究的目的:

调查tRCC中的B7-H3表达及其与mTOR信号的关联.
评估B7-H3作为tRCC的潜在治疗点.

主要方法:

在临床前tRCC模型 (细胞系,小鼠模型) 和人类tRCC样本中评估了B7-H3表达.
利用药理学和基因抑制mTOR信号传递.
分析基因和蛋白质表达水平,包括与正常脏和透明细胞RCC (ccRCC) 的比较.
与临床参数和免疫细胞含量相关的B7-H3表达,使用大量RNAseq解卷.

主要成果:

在tRCC中的TFE3融合蛋白诱导B7-H3上调.
在tRCC模型中,mTOR抑制降低了B7-H3的表达.
人类tRCC的CD276基因表达明显高于正常脏.
与正常脏或ccRCC相比,tRCC的瘤细胞B7-H3强度和比例得分更高.
在转移性tRCC中更高的B7-H3表达与较低的CD4+T细胞含量相关.

结论:

tRCC 融合蛋白通过 mTOR 信号调节 B7-H3.
与正常脏和ccRCC相比,B7-H3在tRCC中显著过度表达.
B7-H3代表了对tRCC的有希望的治疗点,特别是在转移的环境中.

关键词:

B7‐H3 其他 GPNMBMB GPNMB是什么意思 TFE3 TFE3 的时间.美国联邦税务法 (TFEB)在mTOROR中使用mTOR.细胞癌瘤是细胞癌.转位性细胞癌 (tRCC)

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