非小细胞肺癌（NSCLC）是全球癌症死亡的主要原因，由于缺乏针对晚期的有效疗法和能够在进展之前诊断该疾病的标志物而仍是尚未解决的医学问题。针对PD-1 / PD-L1检查站的免疫治疗对许多癌症，包括NSCLC有希望，但其成功取决于PD-L1的肿瘤表达情况。PATZ1是不同恶性肿瘤中新兴的与癌症相关的转录调节因子和诊断/预后生物标志物，但其在肺癌中的作用仍不清楚。在这里，我们研究了PATZ1在NSCLC中的表达和作用，并与NSCLC亚型和PD-L1表达相关联。通过免疫组化技术，对包括肺鳞癌（LUSCs）和腺癌（LUADs）的104例NSCLC进行了回顾性分析，以检测PATZ1和PD-L1的表达情况。结果相互之间和与临床特征相关，一方面表明PATZ1高表达与LUSC亚型呈正相关，另一方面PATZ1与PD-L1呈负相关，独立NSCLC数据集在mRNA水平上得到验证。一致地，两种NSCLC细胞系转染了PATZ1过表达质粒，显示出PD-L1的下调，提示PATZ1在PD-L1的负调节中起作用。我们还表明，PATZ1过表达抑制NSCLC细胞的增殖、迁移和侵袭，并且Patz1-knockout小鼠发展出LUAD。总体而言，这表明PATZ1可能在NSCLC中充当肿瘤抑制剂。

Non-small cell lung cancer (NSCLC), the leading cause of cancer death worldwide, is still an unmet medical problem due to the lack of both effective therapies against advanced stages and markers to allow a diagnosis of the disease at early stages before its progression. Immunotherapy targeting the PD-1/PD-L1 checkpoint is promising for many cancers, including NSCLC, but its success depends on the tumor expression of PD-L1. PATZ1 is an emerging cancer-related transcriptional regulator and diagnostic/prognostic biomarker in different malignant tumors, but its role in lung cancer is still obscure. Here we investigated expression and role of PATZ1 in NSCLC, in correlation with NSCLC subtypes and PD-L1 expression. A cohort of 104 NSCLCs, including lung squamous cell carcinomas (LUSCs) and adenocarcinomas (LUADs), was retrospectively analyzed by immunohistochemistry for the expression of PATZ1 and PD-L1. The results were correlated with each other and with the clinical characteristics, showing on the one hand a positive correlation between the high expression of PATZ1 and the LUSC subtype and, on the other hand, a negative correlation between PATZ1 and PD-L1, validated at the mRNA level in independent NSCLC datasets. Consistently, two NSCLC cell lines transfected with a PATZ1-overexpressing plasmid showed PD-L1 downregulation, suggesting a role for PATZ1 in the negative regulation of PD-L1. We also showed that PATZ1 overexpression inhibits NSCLC cell proliferation, migration, and invasion, and that Patz1-knockout mice develop LUAD. Overall, this suggests that PATZ1 may act as a tumor suppressor in NSCLC.