Serum AFU, GGT and TK1 levels in PHC patients and their correlation with clinicopathology and diagnostic value.

To investigate the expression level and clinical significance of fucosidase (AFU), glutamyltranspeptidase (GGT), and thymidine kinase 1 (TK1) in the serum of patients with primary liver cancer (PHC). A total of 135 PHC patients in Baoji Central Hospital from September 2014 to February 2018 were selected as a research group (RG), while 127 healthy subjects were collected as a control group (CG). Enzyme-linked immunosorbent assay (ELISA) was used to detect the AFU, GGT, and TK1 concentrations in serum of the two groups, and the diagnostic value of combined detection of the three for PHC was analyzed. AFU, GGT, and TK1 concentrations in serum of the RG were dramatically higher than those of the CG (P< 0.050). ROC curve analysis showed that the sensitivity of AFU, GGT, and TK1 in the single diagnosis of PHC was 88.00, 94.00, and 66.00% respectively, and the specificity was 68.00, 54.00, and 66.00% respectively. The sensitivity and specificity of the combined diagnosis of PHC were 76.00 and 90.00%, respectively. AFU, GGT, and TK1 concentrations were different in the presence or absence of liver cirrhosis, TNM stage, and tissue type (P< 0.050). AFU, GGT, and TK1 concentrations in PHC patients were dramatically higher than those in healthy people. Combined detection of the three has good diagnostic value for PHC.

Metformin enhances the chemosensitivity of hepatocarcinoma cells to cisplatin through AMPK pathway.

This study investigated the effect of metformin on chemosensitivity of hepatocarcinoma cells to cisplatin and the possible mechanism. HepG2 and Huh-7 hepatoma cells were treated with cisplatin at concentrations of 0, 2, 4, 6, 8 and 10 µM for 48 h. Proliferation of HepG2 and Huh-7 hepatoma cells were detected by MTT assay. Apoptosis of hepatocellular carcinoma cells was detected by flow cytometry. Western blot analysis was used to detect the expression of 5-monophosphate-activated protein kinase (AMPK) and p-AMPK protein. Proliferative activity of HepG2 and Huh-7 cells decreased with the increase of cisplatin concentration. After adding metformin, proliferation ability of hepatocarcinoma cells was significantly reduced. Apoptosis rate of the metformin was significantly higher than that of the control group, and apoptosis rate of the cisplatin + metformin was significantly higher than that of the cisplatin group. There was no significant difference in expression level of AMPK protein found between control, metformin, cisplatin and cisplatin + metformin group. Compared with the control, ratio of p-AMPK/AMPK in metformin group was increased, and ratio of p-AMPK/AMPK in cisplatin + metformin was significantly higher than that in cisplatin group. Activity of cells in cisplatin + metformin + compound C (AMPK pathway blocker) group was significantly higher than that of cisplatin + metformin, while apoptosis of cells in cisplatin + metformin + compound C (AMPK pathway blocker) was significantly lower than that of cisplatin + metformin group. In conclusion, metformin can inhibit the proliferation, promote apoptosis and enhance the chemosensitivity of hepatocarcinoma cells to cisplatin through AMPK pathway.