| Description: |
Gambogenic acid is an inhibitor of the FGFR signaling pathway in erlotinib-resistant non-small-cell lung cancer (NSCLC) and exhibits anti-tumor effects, it can cause aberrant autophagy to induce cell death and may suggest the potential application of Gambogenic acid as a tool or viable drug in anticancer therapies.Gambogenic acid could inhibit the proliferation of melanoma B16 cells and induce their apoptosis within certain time and concentration ranges. Its mechanism in inducing the cell apoptosis may be related to PI3K/Akt/mTOR signaling pathways. |
| Targets: |
Caspase | ROS | PI3K | Akt | mTOR | MMP(e.g.TIMP) | Bcl-2/Bax | FGFR | Autophagy |
| In vitro: |
| Zhong Yao Cai. 2014 Mar;37(3):469-73. | | Apoptosis of melanoma B16 cells induced by gambogenic acid.[Pubmed: 25174115] | To study the inhibitory effect of Gambogenic acid (GNA) on melanoma B16 cells proliferation, and to explore the role of cell apoptosis.
METHODS AND RESULTS:
The inhibitory effect of Gambogenic acid on the proliferation of B16 cells was measured by methyl thiazolyl tetrazolium (MTT) assay; Alternation of B16 cells ultrastructure was detected by AO/EB staining under fluorescent microscope; Flow cytometry was used to detect intracellular reactive oxygen species (ROS) in B16 cells generated by Gambogenic acid treatment Western blotting was used to investigate the expression of intracellular Caspase-3 proteins changes. MTT results showed that the Gambogenic acid within a certain time and a certain concentration significantly suppressed the proliferation of B16 cells and morphological changes were observed by fluorescence microscope on B16 cells after Gambogenic acid treatment. AO/EB staining showed that the major cell density decreased. Gambogenic acid treated cells showed obvious apoptotic status. After the cells treated with Gambogenic acid, in a short period of time, intracellular ROS levels increased dramatically compared with the control group (P < 0.01), and the mitochondrial membrane had a low potential consistently. Western blotting results showed that changes of intracellular proteins expression in the release of Caspase-3 proteins expression levels were increased after Gambogenic acid treatment.
CONCLUSIONS:
Gambogenic acid can inhibit malignant melanoma B16 cells growth and proliferation and induce apoptosis within a certain time and at a certain concentration. |
|
| In vivo: |
| Asian Pac J Cancer Prev. 2013;14(12):7601-5. | | Gambogenic acid induction of apoptosis in a breast cancer cell line.[Pubmed: 24460340] | 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 AND RESULTS:
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. 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.
CONCLUSIONS:
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. |
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