INVESTIGATING THE IMPACT OF CISPLATIN-REGULATED PD-L1 ON PBMCS AND ITS INFLUENCE ON GASTRIC CANCER CELL PROLIFERATION IN ATHLETES
Keywords:
cisplatin; programmed death factor ligand 1; peripheral blood mononuclear cells; gastric cancer SGC-7901 cells; proliferationAbstract
Objective: This study investigates the impact of cisplatin on PD-L1 expression in peripheral blood mononuclear cells (PBMCs) and its subsequent effects on the proliferation of SGC-7901 gastric cancer cells in an athletic population. Method: We employed the SGC-7901 gastric cancer cell line to explore the effects of varying concentrations of cisplatin (0, 0.5, 1.0, and 2.0 µg/ml). The CCK-8 assay was used to assess cell proliferation inhibition. Additionally, flow cytometry analyzed cell apoptosis, changes in PD-L1 expression on the surface of cancer cells, and lymphocyte apoptosis post-co-incubation with PBMCs. Results: Significant inhibition of SGC-7901 cell proliferation was observed in response to increasing concentrations of cisplatin, with notably higher rates at 0.5, 1.0, and 2.0 µg/ml compared to the control (P<0.05). Apoptotic rates also increased correspondingly, with the highest PD-L1 expression observed at 1.0 µg/ml. Notably, the apoptosis rates of CD4+ and CD8+ T-cells were elevated in groups exposed to higher cisplatin doses, indicating enhanced immunogenic cell death. Conclusion: Cisplatin effectively enhances PD-L1 expression on gastric cancer cells, potentially modulating the immune response in athletes. These findings suggest that the immunomodulatory effects of cisplatin could differ in athletes due to their unique physiological profiles, influencing the efficacy of treatments and subsequent immune responses. The study highlights the need for tailored therapeutic strategies that consider the distinct biochemical and immunological environments of athletes undergoing cancer treatment. This approach could optimize treatment efficacy and better manage the side effects associated with conventional chemotherapy in athletic individuals.