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Acta Pharmacologica Sinica 2007 March; 28 (3): 446-452; doi: 10.1111/j.1745-7254.2007.00536.x |
| Original Article | [ Full text ] |
| Mechanisms of antiprostate cancer by gum mastic: NF-κB signal as target1 |
Mei-lan HE2,4, Ang LI2, Chun-su XU2, Shun-li WANG3, Meng-jie ZHANG2, Hua GU2, Yao-qin YANG3, Hui-hong TAO3 2Institute of Cancer Research, Life Science and Technology School, Tongji University, Shanghai 200092, China; 3Cellular Morphology Center, Medical School, Tongji University, Shanghai 200092, China |
Methods: 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and a flow cytometer were used to detect the effect of gum mastic on the proliferation of PC-3 cells. Then, reporter gene assay, RT-PCR, and Western blotting were carried out to study the effects of gum mastic on the NF-κB protein level and the NF-κB signal pathway. The expression of genes involved in the NF-κB signal pathway, including cyclin D1, inhibitors of κBs (IκBα), and phosphorylated Akt (p-AKT), were measured. In addition, transient transfection assays with the 5× NF-κB consensus sequence promoter was also used to test the effects of gum mastic.
Results: Gum mastic inhibited PC-3 cell growth and blocked the PC-3 cell cycle in the G1 phase. Gum mastic also suppressed NF-κB activity in the PC-3 cells. The expression of cyclin D1, a crucial cell cycle regulator and an NF-κB downstream target gene, was reduced as well. Moreover, gum mastic decreased the p-AKT protein level and increased the IκBα protein level.
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Keywords: gum mastic; prostate cancer; NF-κB signal |
| 1 Project supported by the Tongji University Medical Grant (No 2000219015). |
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