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Li, Qing; Zhang, Liren; You, Wenhua; Xu, Jiali; Dai, Jingjing; Hua, Dongxu; Zhang, Ruizhi; Yao, Feifan; Zhou, Suiqing; Huang, Wei; Dai, Yongjiu; Zhang, Yu; Baheti, Tasiken; Qian, Xiaofeng; Pu, Liyong; Xu, Jing; Xia, Yongxiang; Zhang, Chuanyong; Tang, Jinhai; Wang, Xuehao
Nature communications, 12/2022, Volume: 13, Issue: 1Journal Article
Programmed death receptor-1 (PD-1) blockade have achieved some efficacy but only in a fraction of patients with hepatocellular carcinoma (HCC). Programmed cell death 1 ligand 1 (PD-L1) binds to its receptor PD1 on T cells to dampen antigen-tumor immune responses. However, the mechanisms underlying PD-L1 regulation are not fully elucidated. Herein, we identify that tumoral Prdm1 overexpression inhibits cell growth in immune-deficient mouse models. Further, tumoral Prdm1 overexpression upregulates PD-L1 levels, dampening anti-tumor immunity in vivo, and neutralizes the anti-tumor efficacy of Prdm1 overexpression in immune-competent mouse models. Mechanistically, PRDM1 enhances USP22 transcription, thus reducing SPI1 protein degradation through deubiquitination, which enhances PD-L1 transcription. Functionally, PD-1 mAb treatment reinforces the efficacy of Prdm1-overexpressing HCC immune-competent mouse models. Collectively, we demonstrate that the PRDM1-USP22-SPI1 axis regulates PD-L1 levels, resulting in infiltrated CD8 T cell exhaustion. Furthermore, PRDM1 overexpression combined with PD-(L)1 mAb treatment provides a therapeutic strategy for HCC treatment.
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