新型去泛素酶与含泛素的新型 DUB 家族 1 (MINDY1) 相互作用的基序在肝癌组织中高表达，在维持肝癌细胞的干性中发挥着至关重要的作用。程序性死亡配体-1 (PD-L1) 是肿瘤细胞过度表达的免疫抑制分子。 MINDY1 通过去泛素化 PD-L1 抑制肝癌细胞干性的潜在作用尚未见报道。为了研究 MINDY1 通过调节 PD-L1 泛素化介导肝癌免疫逃逸的机制，我们利用蛋白印迹技术检测了 50 例肝细胞癌 (HCC) 患者的肝癌及癌旁组织中 MINDY1 和 PD-L1 的表达水平和免疫组织化学。我们分析了肝癌组织中MINDY1和PD-L1的表达水平及其与患者5年无瘤生存率的相关性。随后，使用小干扰 RNA (siRNA) 干扰在 Huh7 细胞中敲低 MINDY1 表达，或通过转染 MINDY1 过表达质粒来上调 MINDY1 表达。评估 MINDY1 敲低或过表达对 HCC 细胞增殖、凋亡、迁移和侵袭的影响，以及 PD-L1 结合和泛素化的调节。 MINDY1 高表达组和 PD-L1 高表达组的 5 年无瘤生存率均显着较低（χ2 = 4.919 和 13.158）。 MINDY1 高表达组和低表达组之间的生存率存在显着差异 (χ2= 27.415)。 MINDY1被发现与PD-L1直接相互作用，MINDY1基因敲除促进PD-L1泛素化，MINDY1过表达抑制PD-L1泛素化。所有比较均产生具有统计学意义的结果（P < 0.05）。总之，MINDY1通过抑制PD-L1泛素化和介导免疫逃逸来抑制肝癌的恶性进展。

The novel deubiquitinase enzyme, motif interacting with ubiquitin-containing novel DUB family-1 (MINDY1), is highly expressed in liver cancer tissues and plays a crucial role in maintaining the stemness of liver cancer cells. Programmed death ligand-1 (PD-L1) is an immunosuppressive molecule overexpressed by tumour cells. The potential role of MINDY1 in inhibiting the stemness of liver cancer cells by deubiquitinating PD-L1 has not yet been reported. To investigate the mechanism by which MINDY1 mediates immune escape in liver cancer through the regulation of PD-L1 ubiquitination, we examined the expression levels of MINDY1 and PD-L1 in liver cancer and adjacent tissues from 50 hepatocellular carcinoma (HCC) patients using protein imprinting and immunohistochemistry. We analyzed the relationship between the expression levels of MINDY1 and PD-L1 in liver cancer tissues and their correlation with the 5-year tumor-free survival rates of patients. Subsequently, MINDY1 expression was knocked down in Huh7 cells using small interfering RNA (siRNA) interference or upregulated through transfection with a MINDY1 overexpression plasmid. The effects of MINDY1 knockdown or overexpression on the proliferation, apoptosis, migration, and invasion of HCC cells, as well as the regulation of PD-L1 binding and ubiquitination, were assessed. The 5-year tumor-free survival rates were significantly lower in both the high MINDY1 expression group and the high PD-L1 expression group (χ2 = 4.919 and 13.158, respectively). A significant difference in survival was observed between the high and low MINDY1 expression groups (χ2= 27.415). MINDY1 was found to directly interact with PD-L1, with MINDY1 gene knockdown promoting PD-L1 ubiquitination and MINDY1 overexpression inhibiting PD-L1 ubiquitination. All comparisons yielded statistically significant results (P < 0.05). In conclusion, MINDY1 inhibits the malignant progression of liver cancer by inhibiting PD-L1 ubiquitination and mediating immune escape.