The effect of Sennoside A on malignant biological behavior of gallbladder cancer cells and the related mechanism
10.3760/cma.j.cn113884-20240119-00024
- VernacularTitle:番泻苷A对胆囊癌细胞恶性生物学行为的影响及相关机制
- Author:
Shanshan LI
1
;
Hongyu JIA
;
Lili YAN
;
Meimei XU
Author Information
1. 秦皇岛市第一医院消化内科，秦皇岛 066000
- Keywords:
Gallbladder neoplasms;
Sennoside A;
Phosphatidylinositol 3-kinase/kinase B pathway;
Glycolysis
- From:
Chinese Journal of Hepatobiliary Surgery
2024;30(7):537-543
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the effects of Sennoside A (SA) on the proliferation, migration, invasion, glycolysis and other malignant biological behaviors of gallbladder carcinoma cells, and to analyze the related mechanisms.Methods:Human gallbladder carcinoma cell lines, NOZ and SGC-996, were cultured in vitro and divided into control group, SA low dose group (L-SA, 25 μmol/L), SA medium dose group (M-SA, 50 μmol/L) and SA high dose group (H-SA, 100 μmol/L), and H-SA+ phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) signaling pathway activator 740Y-P group, respectively. The proliferation, migration, invasion, apoptosis and glycolysis of gallbladder cancer cells in each group were detected by cell counting assay, Transwell, flow cytometry and glycolysis kit. The protein levels of PI3K, p-PI3K, AKT and p-AKT were detected by Western blot assay. NOZ cells were used to construct tumor model of nude mice, and the mice were divided into saline treatment group and 10 mg/kg SA treatment group. The tumor formation ability of the two groups of mice was compared, and the expression level of Ki-67 in tumor of the two groups was detected by immunohistochemical assay.Results:Compared with control group, the proliferation, migration, invasion, glycolysis ability, the expression levels of p-PI3K and p-AKT were significantly decreased in SA treatment groups, while the apoptosis level was significantly up-regulated, all differences were statistically significant ( P<0.05). Compared with H-SA group, the proliferation, migration, invasion and glycolysis of H-SA+ 740Y-P group cells were up-regulated, while the apoptosis level was significantly decreased, all differences were statistically significant ( P<0.05). In vivo tumorigenesis experiments showed that, compared with the control group, the tumor volume of the SA-treated mice was reduced at day 28 [(1 051.32±130.29) mm 3 vs (575.07±170.54) mm 3, P=0.0003), the tumor weight was reduced [(1.04±0.24) g vs (0.58±0.13) g, P=0.0019], and the average optical density of Ki-67 expression was reduced [(77.00±7.00) vs (33.33±7.51), P=0.0018]. Conclusion:SA can inhibit the proliferation, migration, invasion and glycolysis of gallbladder carcinoma cells by regulating PI3K/AKT pathway.
