Gambogic Acid Induces Apoptosis in Raji Lymphoma Cells Via Gfi-1/STAT5 Signaling.
TL;DR
The findings suggest that gambogic acid inhibits the STAT5 pathway by regulating the Gfi-1 gene through promoting apoptosis in Raji cells, suggesting that the anti-cancer mechanism of gambogic acid on Raji cells is influenced by the STAT5 pathway.
Abstract
To understand the role of gambogic acid in regulating apoptosis in Raji cells, experiments were performed to examine the signaling pathways. The study was carried out using a cell growth inhibition assay to detect the activity changes of Raji cells, as well as analyzing the regulatory process of apoptosis and regulatory genes through the cell apoptosis assay. To detect the changes in regulatory genes of Raji cells after treatment, experimental groups with different doses and concentrations of gambogic acid were assigned. The interference experiment was designed to investigate the regulatory mechanism of gambogic acid on the apoptosis process of Raji cells. The experiments with dose-response showed that gambogic acid achieved the highest inhibition of cell proliferation at concentrations of 0-2 µM. The treatment duration of 12-24 h was identified as the optimal treatment. In apoptosis assays (24 h), total apoptotic rates increased to 13.28% ± 0.52%, 22.55% ± 0.71%, and 40.52% ± 1.02% following gambogic acid treatment at 0.25, 0.5, 1.0 µg/mL respectively, compared with 4.98% ± 0.19% in the control group (p < 0.05). The expression of the Gfi-1 (Growth Factor Independent 1) gene was suppressed in gambogic acid-treated cells (p < 0.05), while gambogic acid markedly upregulated the apoptotic protein cleaved caspase-3. These findings suggest that Gambogic acid inhibits the STAT5 pathway by regulating the Gfi-1 gene through promoting apoptosis in Raji cells. Therefore, the anti-cancer mechanism of gambogic acid on Raji cells is influenced by the STAT5 pathway.