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时间调节PD-L1表达,并在乳腺癌中发挥免疫抑制作用

Xinrui Dong¹, Huijuan Dai², Yanping Lin¹

¹Department of Breast Surgery, Renji Hospital, School of Medicine, Shanghai Jiaotong University, No. 1630 Dongfang Road, Shanghai, 200127, China.

Journal of translational medicine

|June 20, 2023

概括

昼夜基因 TIMELESS (TIM) 通过通过c-Myc相互作用对PD-L1进行上调来促进乳腺癌的进展. TIM knockdown可以增强抗瘤免疫力,这表明TIM是免疫治疗的治疗标和生物标志物.

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:

对瘤的PD-L1 (CD274) 上调促进免疫逃逸,限制了乳腺癌等癌症的免疫治疗疗效.
在癌症中导致高PD-L1水平的机制尚不完全理解.

研究的目的:

研究 TIMELESS (TIM) 在乳腺癌进展中的作用及其与PD-L1表达和CD8+ T细胞透的关联.
阐明TIM影响PD-L1转录和乳腺癌攻击性的分子机制.

主要方法:

来自TIM-knockdown乳腺癌细胞和公共数据集的RNA测序数据的生物信息分析.
在乳腺癌细胞系中的体内和体外实验.
在人类乳腺癌样本中评估TIM表达,PD-L1水平和CD8+T细胞透.

主要成果:

在乳腺癌中,TIM表达与CD8+T细胞透相反相关.
提姆抗击增强了CD8+T细胞的抗瘤活性.
蒂姆与c-Myc相互作用,增加PD-L1转录,促进乳腺癌的攻击性和进展.
高TIM水平与PD-L1抑制剂治疗的积极反应相关.

结论:

通过与c-Myc的相互作用,提升PD-L1的调节,促进TIM促进乳腺癌,这有助于免疫逃避.
TIM是乳腺癌治疗的潜在治疗标.
TIM作为一个有前途的生物标志物,用于预测患者对抗PD-L1免疫疗法的反应.

关键词:

乳腺癌是什么? 乳腺癌是什么 CD8+ T 淋巴细胞在PD-L1中.无时无刻的时间.

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