肺癌是目前全世界范围内最常见的威胁人类生命的恶性肿瘤之一。许多肿瘤细胞系，包括肺癌细胞，都高表达PD-L1分子，其与淋巴细胞表面的PD-1分子结合后，可削弱机体的抗肿瘤免疫应答，从而导致肿瘤免疫逃逸的发生。降低PD-L1在肿瘤细胞表面的表达可以减少其与PD-1的结合，阻断负向调控信号，使T细胞恢复活性，从而增强免疫应答。影响PD-L1表达的机制研究主要集中在翻译后修饰（比如磷酸化，糖基化和泛素化）和转录调控上，靶向PD-L1的翻译后修饰可以增强抗肿瘤的免疫应答。我们的研究发现肺癌细胞系中PD-L1受到乙酰化的调控，随后的机制研究证实乙酰化可以抑制PD-L1的泛素化降解及剪切脱落。后续我们将明确乙酰化对PD-L1表达的调控机制及对肿瘤细胞生物学行为和免疫功能的影响，并用小鼠模型和临床肺癌样品验证其体内功能，从而阐明其与肺癌发生发展的关系，为肺癌的临床治疗提供新思路和新策略。

Lung cancer is one of the most frequent malignant tumors in the world and has a poor prognosis. Studies have shown that PD-L1 is overexpressed in various cancers including lung cancer, indicating the important role of PD-L1 in cancer development. Antibody-mediated blockade of the interaction between PD-1 on CTLs and PD-L1 on tumor cells, which inactivates the tumoricidal activity of CTLs and allows tumor cell immune evasion, has exhibited significant clinical efficacy in several types of cancer, including advanced lung cancer. Reported results suggested that PD-L1 mediated immunosuppression is extensively regulated by posttranslational modifications (PTMs) and transcriptional regulation of PD-L1. Protein glycosylation, phosphorylation, and ubiquitination affected PD-L1 protein stability and regulated antitumor immune responses. Targeting PD-L1 PTMs may be a novel strategy for enhancing anti-tumor immune responses. Our preliminary data found that PD-L1 is regulated by acetylation in lung cancer cells. Further study indicated PD-L1 acetylation may control its degradation and shed. Our study can provide not only the insight into the molecular regulation mechanism and function of acetylation on PD-L1 but also the new target for cancer therapy.