Mechanism of anticancer effect of gambogic acid on gastric signet ring cell carcinoma
Date
16. 08. 20Metadata
Show full item recordAbstract
Gambogic acid has demonstrated inhibitory effects on the growth of various cancer cell types, such as breast cancer, pancreatic
cancer, prostate cancer, lung cancer, and osteosarcoma. This study aims to investigate the antiproliferative activity of
Gambogic acid on SNU-16 cells derived from gastric signet ring cell carcinoma and elucidate the underlying mechanisms.
The cytotoxic effect of gambogic acid was evaluated in SNU-16 cells by treating them with different concentrations of the
compound, and the XTT cell viability assay was employed to assess cell viability. ELISA was used to measure bax, BCL-
2, caspase 3, PARP, and 8-oxo-dG levels. Additionally, immunofluorescence staining was applied to assess 8-oxo-dG and
LC3β levels in SNU-16 cells. It was observed that gambogic acid exerted a dose-dependent and statistically significant antiproliferative
effect on SNU-16 cells. The IC50
value of gambogic acid in SNU-16 cells was found to be 655.1 nM for 24 h.
Subsequent investigations conducted using the IC50
dose revealed a significant upregulation of apoptotic proteins including
cleaved caspase 3, Bax, and cleaved PARP (p < 0.001), along with a downregulation of BCL-2 (p < 0.001), an anti-apoptotic
protein. Moreover, the administration of this drug led to an upregulation of 8-oxo-dG (p < 0.001), a widely acknowledged
biomarker indicating oxidative damage in DNA, as well as an increase in LC3β levels (p < 0.05), a marker associated with
autophagy. The antiproliferative effect of gambogic acid against gastric signet ring cell carcinoma is attributed to its ability
to induce apoptosis and autophagy. This discovery highlights the promising potential of gambogic acid as a treatment option
for gastric signet ring cell carcinoma.