OBJECTIVE： To investigate the anti-breast cancer （BC） effects and mechanisms of action of Xihuang pill （XHP） by conducting in vitro experiments on hu- man BC cell lines. METHODS： Two human BC cell lines （MCF-7 ...OBJECTIVE： To investigate the anti-breast cancer （BC） effects and mechanisms of action of Xihuang pill （XHP） by conducting in vitro experiments on hu- man BC cell lines. METHODS： Two human BC cell lines （MCF-7 and MDA- MB231） were cultured and treated with XHP. Cell viability was detected using the 3-（4, 5-Dimeth- ylthiazol-2-yl）-2, 5-diphenyltetrazolium bromide （MTT） assay. Flow cytometry was used to measure the cell cycle and apoptosis. The cell cycle was ana- lyzed with propidium iodide staining. Apoptosis was evaluated using the Annexin V-fluorescein iso- thiocyanate/propidium iodide method. Western blotting was used to analyze the expression of es- trogen receptor （ER）-α and ER-13.RESULTS： XHP had growth-inhibitory effects on MCF-7 and MDA-MB231 cells with a half-maximal inhibitory concentration （IC50） of 10.14 mg/mL （MCF-7） and 8.98 mg/mL （MDA-MB231）. Apoptosis was induced to some extent. Certain changes in the ER were caused. Upregulation of ER-a protein was found in MCF-7 cells. ER-β expression in MDA-MB231 cells was increased. Cell-cycle arrest was not observed in the two BC cell lines. ER-β ex- pression in MCF-7 cells was unchanged. No ER-a ex- pression was shown in MDA-MB231 cells. CONCLUSION： These data suggest that XHP can af- fect cell viability and cause apoptosis, but that the cell cycle is not blocked. XHP has a certain impact on ER expression, but its mechanisms of action of anti-13C effects may not be due to regulation of ER expression.展开更多
基金Supported by the Beijing Traditional Chinese Medicine Science and Technology Project(QN2010-3)National Natural Science Foundation of China(No.81001564)
文摘OBJECTIVE： To investigate the anti-breast cancer （BC） effects and mechanisms of action of Xihuang pill （XHP） by conducting in vitro experiments on hu- man BC cell lines. METHODS： Two human BC cell lines （MCF-7 and MDA- MB231） were cultured and treated with XHP. Cell viability was detected using the 3-（4, 5-Dimeth- ylthiazol-2-yl）-2, 5-diphenyltetrazolium bromide （MTT） assay. Flow cytometry was used to measure the cell cycle and apoptosis. The cell cycle was ana- lyzed with propidium iodide staining. Apoptosis was evaluated using the Annexin V-fluorescein iso- thiocyanate/propidium iodide method. Western blotting was used to analyze the expression of es- trogen receptor （ER）-α and ER-13.RESULTS： XHP had growth-inhibitory effects on MCF-7 and MDA-MB231 cells with a half-maximal inhibitory concentration （IC50） of 10.14 mg/mL （MCF-7） and 8.98 mg/mL （MDA-MB231）. Apoptosis was induced to some extent. Certain changes in the ER were caused. Upregulation of ER-a protein was found in MCF-7 cells. ER-β expression in MDA-MB231 cells was increased. Cell-cycle arrest was not observed in the two BC cell lines. ER-β ex- pression in MCF-7 cells was unchanged. No ER-a ex- pression was shown in MDA-MB231 cells. CONCLUSION： These data suggest that XHP can af- fect cell viability and cause apoptosis, but that the cell cycle is not blocked. XHP has a certain impact on ER expression, but its mechanisms of action of anti-13C effects may not be due to regulation of ER expression.
