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Archive > Volume 30 Issue 10 > 2023,30(10):874-880. DOI:10.3872/j.issn.1007-385X.2023.10.004 Prev Next
Basic Research
Ginkgolide B inhibits the malignant biological behaviors of gastric cancer HGC-27 cells by blocking the PI3K/Akt/mTOR signaling pathway
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Abstract:
Objective: To investigate whether ginkgolide B (GKB) inhibits the proliferation, apoptosis, migration and invasion of gastric cancer HGC-27 cells by blocking the PI3K/Akt/mTOR signaling pathway. Methods: Gastric cancer HGC-27 cells were divided into control group, low-dose GKB (100 mg/L) group, high-dose GKB (200 mg/L) group, high-dose GKB (200 mg/L)+740Y-P (PI3K activator) group, and Ly294002 (PI3K inhibitor) group. MTT and Edu, FCM, Transwell tests were used to detect the proliferation, apoptosis, migration and invasion abilities of HGC-27 cells in each group. The expressions of PI3K mRNA, Akt mRNA, mTOR mRNA, and the protein expressions of Ki-67, caspase-3, p-PI3K/PI3K, p-Akt/Akt, and p-mTOR/mTOR in cells of each group were detected by qPCR and Western blotting. A nude mouse transplanted tumor model of gastric cancer HGC-27 cells was established. The effect of GKB on the growth of transplanted tumors was observed. Wesern blotting was used to detect the protein expressions of Ki-67, caspase-3, p-PI3K/PI3K, p-Akt/Akt, and p-mTOR/mTOR in transplanted tumor tissues. Results: The results of in vitro experiments indicated that, compared with the control group, the proliferative activity, cell proliferation rate, the numbers of cell migration and invasion, the expression levels of PI3K mRNA, Akt mRNA and mTOR mRNA, and the protein expression levels of Ki-67, p-PI3K/PI3K, p-Akt/Akt, p-mTOR/mTOR of HGC-27 cells in low-dose GKB group, high-dose GKB group and Ly294002 group, reduced significantly (all P<0.05). The apoptosis rate and the expression of caspase-3 protein increased significantly (all P<0.05). 740Y-P could partially reverse the inhibitory effect of GKB on HGC-27 cells (all P<0.05). Tumor-bearing nude mouse experience showed that GKB could significantly inhibit the growth of nude mouse transplanted tumors of HGC-27 cells (P<0.05) and downregulate the expressions of PI3K/Akt/mTOR pathway-related proteins. Conclusion: GKB may inhibit the proliferation, migration and invasion and promote the apoptosis of gastric cancer HGC-27 cells by blocking the PI3K/Akt/mTOR signaling pathway.
Keywords:
ginkgolide B (GKB) ; gastric cancer ; HGC-27 cell ; PI3K/Akt/mTOR signaling pathway ; proliferation ; migration ; apoptosis
