Effects of Sauchinone on the Malignant Biological Behaviors and Immune Suppression of Esophageal Cancer Cells by Regulating the PD-1/PD-L1 Signaling Pathway
LUO Qing, LIU Mingwei*
The objective of this study was to investigate the effects of Sau (sauchinone) on the malignant biological behaviors and immune suppression of esophageal cancer cells, and its regulatory mechanism on the PD-1/PD-L1 signaling pathway. Human esophageal cancer cells KYSE-510 and normal esophageal epithelial cell line Het-1A were cultured and treated with different concentrations of Sau. The cell survival rate was detected by CCK-8 method. KYSE-510 cells were randomly separated into KYSE-510 group, Sau low-concentration (Sau-L) group, Sau medium-concentration (Sau-M) group, Sau high-concentration (Sau-H) group, and Sau-H+pcDNAPD-1 group. CCK-8 method was applied to detect the survival rate of KYSE-510 cells. Plate cloning experiment was applied to detect the clonogenesis ability of KYSE-510 cells. Transwell experiment was applied to detect themigration and invasion abilities of KYSE-510 cells. Flow cytometry was applied to detect the apoptosis of KYSE-510 cells. Western blot was applied to detect the relative expression levels of PD-1/PD-L1 signaling pathwayrelated proteins, VEGF (vascular endothelial growth factor), and TGF-β1 (transforming growth factor-β1). The results showed that the inhibitory effect of Sau on the proliferation of KYSE-510 cells was more significant than that of Het-1A. Compared with the KYSE-510 group, the cell survival rate, clone formation quantity, migration and invasion cell numbers, the protein expression levels of PD-1, PD-L1, VEGF, and TGF-β1 in the Sau-L, Sau-M, and Sau-H groups all reduced (P<0.05), while the cell apoptosis rate increased (P<0.05). However, overexpression of PD-1 in KYSE-510 cells treated with high concentration of Sau reversed the trend of changes of the above indicators (P<0.05). In conclusion, Sau can inhibit the malignant biological behaviors of esophageal cancer cells, relieve immune suppression, and its mechanism may be related to the inhibition of the PD-1/PD-L1 signaling pathway.
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