Gambogenic Acid Induction of Apoptosis in a Breast Cancer Cell Line

Abstract

Background: Gambogenic acid is a major active compound of gamboge which exudes from the Garcinia hanburyi tree. Gambogenic acid anti-cancer activity in vitro has been reported in several studies, including an A549 nude mouse model. However, the mechanisms of action remain unclear. Methods: We used nude mouse models to detect the effect of gambogenic acid on breast tumors, analyzing expression of apoptosis-related proteins in vivo by Western blotting. Effects on cell proliferation, apoptosis and apoptosis-related proteins in MDA-MB-231 cells were detected by MTT, flow cytometry and Western blotting. Inhibitors of caspase-3,-8,-9 were also used to detect effects on caspase family members. Results: We found that gambogenic acid suppressed breast tumor growth in vivo, in association with increased expression of Fas and cleaved caspase-3,-8,-9 and bax, as well as decrease in the anti-apoptotic protein bcl-2. Gambogenic acid inhibited cell proliferation and induced cell apoptosis in a concentration-dependent manner. Conclusion: Our observations suggested that Gambogenic acid suppressed breast cancer MDA-MB-231 cell growth by mediating apoptosis through death receptor and mitochondrial pathways in vivo and in vitro.

Nanosuspensions as delivery system for gambogenic acid: characterization and in vitro/in vivo evaluation

“…Its main active components includes gambogenic acid (GNA, Figure 1a) and gamboge acid (GA, Figure 1b), and GNA exhibits stronger and broader pharmacological activities (Zhou et al, 2008). Previous studies have confirmed that GNA has a broad spectrum anti-tumor effect in breast cancer cell line, lung cancer cells and other cancer cells (Fan et al, 2013;Zhou et al, 2013;Wang et al, 2014). However, the poor solubility, short biological half-life and excessive vascular irritation of GNA hindered its clinical application (Hua et al, 2015).…”

Enhancement of radiotherapy by ceria nanoparticles modified with neogambogic acid in breast cancer cells

“…[18][19][20] NGA increased the death of S180-Lewis lung cancer, CNE-1 human nasopharyngeal carcinoma, and ascites carcinoma cells in a dose-dependent manner. 21 In the present study, we synthesized CNPs modified with NGA (NGA-CNPs) for increased toxicity and targeting, and NGA-CNPs were tested for their ability to enhance the effectiveness of radiation in killing cancer cells. MCF-7 breast cancer cells were treated with NGA-CNPs in conjunction with radiation; the combined treatment induced cell death to a greater extent than radiation alone, and also activated autophagy and led to cell cycle arrest at the G2/M phase.…”

20(S)-Protopanaxadiol Induces Human Breast Cancer MCF-7 Apoptosis through a Caspase-Mediated Pathway

“…Both extrinsic and intrinsic pathways lead to activation executioner caspase (caspase-3). Caspase-3 activated by caspase-8 (extrinsic pathway) or caspase-9 (intrinsic pathway) induces cell shrinkage, nuclear condensation and DNA fragmentation (Zhou et al, 2013). Here, we showed that 20 (S)-PPD treatment activated caspase-9 and caspase-3 in a dosedependent manner ( Figure 5A).…”