| Objective: To investigate the effect of Gambogic acid on the proliferation and apoptosis of lung cancer A549 cells, and to explore its effect on regulation of STAT3.Methods: MTT assay and flow cytomerty were used to detect the growth inhibition and apoptosis of A549 cells induced by different concentrations of GA. Cell morphological change was observed by microscope.The localization of STAT3 and the expression was determined by confocal laser scanning microscopy.STAT3 mRNA expression was determined by RT-PCR and protein level of STAT3 was revealed by western blot analysis.Results: The results indicated that GA could inhibit the proliferation of the A549 cells significantly and promote apoptosis in a time and dose dependent manner.After treatment with GA for 24h,48h,72h,the IC50 value were (2.81±0.28)umol /L,(1.86±0.01) umol /L and (1.35±0.10)umol/L respectively. Further confirmed by flow cytometry, when 1.5umol/L and 3umol/L of GA were given to the A549 cells for 24h, the apoptotic rates were (24.38±1.42)%, (51.60±3.23)% respectively.The apoptosis rate is (77.09±1.44)% when the concentration of GA was up to 6umol/L.Over expression of STAT3 was found in A549 cells,and was situated mainly in the cytoplasm. Cell morphological change was observed by microscope. In the control group,the cells with round caryon were polygon, thin and flat, and they were fast clingy. In the GA treated groups,with the increase of drug concentration,the cells showed a typical morphological changes of apoptosis, the cells became contracted and poor at clingy;disappear of the ecphyma of the cells, and chromatin condensation.The expression of STAT3 mRNA and STAT3 protein were downregulated in A549 cells treated with GA in a concentration dependent manner. Conclusion: GA can inhibit the growth and promote the apoptosis of human lung adenocarcinoma A549 cells,The molecular mechanism may be due to the downregulating expressions of STAT3. |
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