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Updated: Oct 16, 2025

Identifying PD-1/PD-L1 Inhibitors with Surface Plasmon Resonance Technology
Published on: May 2, 2025
[Cisplatin promotes PD-L1 expression in A549 human lung adenocarcinoma cells via activating the ERK pathway]
Hong Zhu1, Dan Liu1, Shukai Deng2
1Department of Respiration, First Affiliated Hospital of Southwest Medical University, Luzhou 646000, China.
Abstract:
Objective To investigate the effect of cisplatin (DDP) on the expression of programmed death 1 ligand 1 (PD-L1) in human lung adenocarcinoma A549 cells and its possible mechanism. Methods Human lung adenocarcinoma A549 cells were cultured in vitro and treated with (0, 0.5, 1, 2, 4, 8) mg/L of DDP for 24, 36, 48 hours. CCK-8 assay was used to detect the cell proliferation inhibition rate and the half maximal inhibitory concentration (IC50) was calculated. The optimal inhibition time of 48 hours and its IC50 were selected for subsequent experiments. A549 cells were then randomized into four groups: blank control group, group with DDP (IC50), group with 20 μmol/L of mitogen-activated protein kinase kinase inhibitor PD98059, and group with DDP (IC50) combined with 20 μmol/L of PD98059. The cells were cultured for 48 hours. The expression of ERK and p-ERK were detected by Western blotting, and PD-L1 expression was detected by flow cytometry. Results Compared with that in the control group, the expression of PD-L1 in A549 cells treated with DDP was up-regulated in a dose-dependent manner. The optimal time was 48 hours and the IC50 was 3.586 mg/L. Also compared with that in the control group, the expression of p-ERK and PD-L1 in the DDP treatment group increased, and the expression of p-ERK in the group with PD98059 decreased. The expressions of p-ERK and PD-L1 in the group with DDP combined with PD98059 were lower than those in the group with DDP, but higher than those in the group with PD98059. Conclusion DDP up-regulates the expression of PD-L1 in A549 cells by activating the ERK signaling pathway.

