Aspirin attenuates hepatocellular carcinoma progression by inhibiting PD-L1 expression

Abstract

Abstract Background and aims: Aspirin, as a widely used anti-inflammatory drug, has been shown to exert anti-cancer effects in a variety of cancers. PD-L1 is widely expressed in tumor cells and inhibits anti-tumor immunity. This study aims to clarify whether aspirin exerts its anti-HCC effect by inhibiting PD-L1 expression. Methods Thirty male SD rats were randomly divided into the DEN, DEN + ASA, ASA, and control groups. The rats in the DEN and DEN + ASA groups were fed with 0.01% diethylnitrosamine freely to establish a liver cancer model. Rats in the DEN + ASA and ASA groups were treated with aspirin by gavage. The expression of PD-L1 in the liver was detected by Western Blot. Results The tumor number and liver weight ratio in the DEN + ASA group were significantly lower than those in the DEN group (P = 0.006, P = 0.046). Biochemical indexes showed that there were significant differences in all indexes between the DEN and control group (P < 0.05). The levels of DBIL, ALP, and TT in the DEN + ASA group were significantly lower than those in the DEN group (P = 0.038, P = 0.042, P = 0.031). In the DEN group, there was an obvious fibrous capsule around the tumor, and the portal vein was dilated. The pathological changes were mild in the DEN + ASA group. The expression of PD-L1 in the DEN group was significantly higher than that in the other three groups (P < 0.05); Aspirin could significantly inhibit the expression of PD-L1 in liver cancer tissues (P = 0.0495). Conclusions Aspirin can inhibit the progression of hepatocellular carcinoma and reduce tumor burden by targeting PD-L1.