Abstract
Objective To evaluate the effect of propofol on the expression of programmed death-ligand-1(PD-L1) in pancreatic cancer cells and the relationship with NMDA/Ca2+ /calmodulin-dependent protein kinaseⅡ(CaMKⅡ)/hypoxia-inducible factor-1α(HIF-1α) pathway. Methods Human pancreatic cancer cells were divided into 5 groups(n=16 each) by a simple random sampling method: control group(group C), propofol group(group P), KN93(CaMK II inhibitor) group, MK801(NMDA receptor antagonist) group and propofol plus rapastinel(NMDA receptor agonist) group(group PR). Cells were cultured in DMEM supplemented with 10% fetal bovine serum in group C. Cells were incubated for 8 h with 50 μmol/L propofol in group P. Cells were incubated for 8 h with 10 μmol/L KN93 in group KN93. Cells were incubated for 8 h with 500 μmol/L MK801 in group MK801. Cells were incubated for 8 h with 50 μmol/L propofol and 20 μmol/L rapastinel in group PR. After the end of treatment in each group, the cell viability was measured using CCK8 assay, the expression of PD-L1, HIF-1α, CaMKⅡ and phosphorylated CaMKⅡ(p-CaMKⅡ) was detected by Western blot, and intracellular calcium concentrations were determined by Fluo3/AM probe. Results Compared with group C, the cell viability was significantly decreased, the expression of PD-L1, HIF-1α and p-CaMKⅡ was down-regulated, and intracellular calcium concentrations were decreased in P, KN93 and MK801 groups(P 0.05). Compared with group P, the cell viability was significantly enhanced, the expression of PD-L1, HIF-1α and p-CaMKⅡ was up-regulated, and intracellular calcium concentrations were increased in group PR(P<0.05). Conclusion The mechanism by which propofol inhibits the malignant potential of pancreatic cancer cells may be related to inhibiting NMDA/CaMKⅡ/HIF-1α pathway and down-regulating PD-L1 expression. Key words: Propofol; Pancreatic neoplasms; Programmed death-ligand-1; Receptors, N-methyl-D-aspartate; Calcium-calmodulin-dependent protein kinase type 2; Hypoxia-inducible factor 1, alpha subunit
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