Antiproliferative activity of gambogic acid isolated from Garcinia hanburyi in Hep3B and Huh7 cancer cells

• Published in: Oncology reports Vol. 29; no. 5; pp. 1744 - 1750
• Main Authors: LEE, PARRY NGAN HON, HO, WING SHING
• Format: Journal Article
• Language: English
• Published: Greece D.A. Spandidos 01.05.2013; Spandidos Publications UK Ltd
• Subjects: Apoptosis; Apoptosis - drug effects; bcl-2-Associated X Protein - metabolism; cancer; Carcinoma, Hepatocellular - drug therapy; Carcinoma, Hepatocellular - metabolism; caspase; Caspase 8 - metabolism; Cell Line, Tumor; Cell Proliferation - drug effects; Cytochromes c - metabolism; DNA Fragmentation - drug effects; gambogic acid; Garcinia - chemistry; Herbal medicine; Humans; Kinases; Liver cancer; Liver Neoplasms - drug therapy; Liver Neoplasms - metabolism; Medical research; Mitochondria - drug effects; Mitochondria - metabolism; Plant Extracts - pharmacology; Signal Transduction - drug effects; Studies; Tumor Suppressor Protein p53 - metabolism; Xanthones - pharmacology; United States > US
• ISSN: 1021-335X; 1791-2431
• DOI: 10.3892/or.2013.2291

The anticancer activities of gambogic acid (GA) on two hepatocellular carcinoma cells with either p53 deletion (Hep3B) or p53 mutation (Huh7) were investigated in the present study. GA inhibited the growth of Hep3B and Huh7 through similar apoptotic pathways. After treatment of Hep3B and Huh7 with GA for 24 h, the IC50 was determined for both cell lines at 1.8 and 2.2 μM, respectively. The results showed that both cancer cells underwent morphological changes and DNA fragmentation. GA induced apoptosis in the two cell lines through caspases-3/7, -8 and -9 in the mitochondrial pathway. The results suggest that both the caspases in the extrinsic death receptor pathway and the mitochondrial-dependent pathway are involved in the GA-induced cell apoptosis. The inhibitory effects of GA on Hep3B and Huh7 are independent of p53-associated pathway.