Department of Pathology, Chi-Mei Medical Center, Tainan, Taiwan.
Department of Internal Medicine, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, No.138, Shengli Road, North District, Tainan, 704, Taiwan.
Sci Rep. 2023 Mar 9;13(1):3943. doi: 10.1038/s41598-023-30565-4.
The role of Programmed Cell Death Ligand 1 (PD-L1) expression in predicting epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKIs) efficacy remains controversial. Recent studies have highlighted that tumor-intrinsic PD-L1 signaling can be modulated by STAT3, AKT, MET oncogenic pathway, epithelial-mesenchymal transition, or BIM expression. This study aimed to investigate whether these underlying mechanisms affect the prognostic role of PD-L1. We retrospectively enrolled patients with EGFR mutant advanced stage NSCLC who received first-line EGFR-TKI between January 2017 and June 2019, the treatment efficacy of EGFR-TKI was assessed. Kaplan-Meier analysis of progression-free survival (PFS) revealed that patients with high BIM expression had shorter PFS, regardless of PD-L1 expression. This result was also supported by the COX proportional hazard regression analysis. In vitro, we further proved that the knockdown of BIM, instead of PDL1, induced more cell apoptosis following gefitinib treatment. Our data suggest that among the pathways affecting tumor-intrinsic PD-L1 signaling, BIM is potentially the underlying mechanism that affects the role of PD-L1 expression in predicting response to EGFR TKI and mediates cell apoptosis under treatment with gefitinib in EGFR-mutant NSCLC. Further prospective studies are required to validate these results.
程序性死亡配体 1(PD-L1)表达在预测表皮生长因子受体酪氨酸激酶抑制剂(EGFR-TKIs)疗效中的作用仍存在争议。最近的研究强调,肿瘤内在的 PD-L1 信号可以被 STAT3、AKT、MET 致癌通路、上皮-间充质转化或 BIM 表达所调节。本研究旨在探讨这些潜在机制是否影响 PD-L1 的预后作用。我们回顾性纳入了 2017 年 1 月至 2019 年 6 月期间接受一线 EGFR-TKI 治疗的 EGFR 突变晚期 NSCLC 患者,评估 EGFR-TKI 的治疗疗效。无进展生存期(PFS)的 Kaplan-Meier 分析显示,高 BIM 表达的患者 PFS 更短,无论 PD-L1 表达如何。COX 比例风险回归分析也支持这一结果。在体外,我们进一步证明,与 PD-L1 敲低相比,BIM 的敲低可诱导吉非替尼治疗后更多的细胞凋亡。我们的数据表明,在影响肿瘤内在 PD-L1 信号的途径中,BIM 是潜在的机制,它影响 PD-L1 表达在预测 EGFR-TKI 反应中的作用,并介导 EGFR 突变 NSCLC 中吉非替尼治疗下的细胞凋亡。需要进一步的前瞻性研究来验证这些结果。