Objective： To investigate the proliferation effect and its pathway of activin A on Ovarian epithelial cancer cells line OVCAR-3. Methods： OVCAR-3 cells were cultured in vitro and the membrane receptor ActR II was de...Objective： To investigate the proliferation effect and its pathway of activin A on Ovarian epithelial cancer cells line OVCAR-3. Methods： OVCAR-3 cells were cultured in vitro and the membrane receptor ActR II was detected by immunohistochemical method. The OVCAR-3 cells were cultured with 10 ng/ml activin A for 7 d to observe the effects. Activin A at 5, 10, 15 and 20 ng/ml was used separately to treat the OVCAR-3 cancer cells for 24, 48 and 72 h in order to draw the growth proliferation rate curve measured by MTT method. The expression of protein bcl-2 was detected by western-blot. When OVCAR-3 cells were treated with 10 ng/ml activin A and 5 lag/ml DDP for 24, 48 and 72 h, cell apoptosis could be detected by electron microscopy and flow cytometry （FCM）. Results： Positive expression of ActR II was detected. We also found that the proliferation of OVCAR-3 reached to the climax on the 5th day of culture. The experiments showed that the cells treated with activin A increased quickly and grew faster than those in control group. Moreover, OVCAR-3 cells treated with activin A for 48 h proliferated significantly greater than those treated for 24 h or 72 h （P〈0.01）. bcl-2 protein expression increased expression in activin A treated group than in control group （P〈0.05）. Conclusion： Activin A could increase the proliferation of OVCAR-3 cells which may be through bcl-2 anti-apoptosis pathway.展开更多
Objective:To investigate the interaction of p53 with docetaxel and berberine and their anticancer activities against oral squamous cell carcinoma.Methods:The interaction between p53 with docetaxel and berberine was in...Objective:To investigate the interaction of p53 with docetaxel and berberine and their anticancer activities against oral squamous cell carcinoma.Methods:The interaction between p53 with docetaxel and berberine was investigated and their mechanisms of action against oral squamous cell carcinoma were studied.Toxicity studies were performed to determine any toxic impact of the drugs on the vital organs of tested animals.Results:In silico results revealed the molecular interaction of docetaxel and berberine with p53 and the molecules were found to be potential p53 inducers.Docetaxel and berberine inhibited the proliferation of cancer cells in a concentration-dependent manner.Flow cytometry analysis revealed that docetaxel and berberine at IC50 concentrations upregulated the expression of p53 in oral squamous cell carcinoma cells,thus triggering apoptotic cell death.In addition,no toxicity was observed in the liver and kidney tissues of mice after docetaxel and berberine treatment.Conclusions:Docetaxel and berberine significantly suppressed the proliferation of oral cancer cells by activating p53 expression and causing apoptotic cell death.Both compounds can be potential agents for the treatment of oral cancer,with little to no toxicity at the tissue level.展开更多
文摘Objective： To investigate the proliferation effect and its pathway of activin A on Ovarian epithelial cancer cells line OVCAR-3. Methods： OVCAR-3 cells were cultured in vitro and the membrane receptor ActR II was detected by immunohistochemical method. The OVCAR-3 cells were cultured with 10 ng/ml activin A for 7 d to observe the effects. Activin A at 5, 10, 15 and 20 ng/ml was used separately to treat the OVCAR-3 cancer cells for 24, 48 and 72 h in order to draw the growth proliferation rate curve measured by MTT method. The expression of protein bcl-2 was detected by western-blot. When OVCAR-3 cells were treated with 10 ng/ml activin A and 5 lag/ml DDP for 24, 48 and 72 h, cell apoptosis could be detected by electron microscopy and flow cytometry （FCM）. Results： Positive expression of ActR II was detected. We also found that the proliferation of OVCAR-3 reached to the climax on the 5th day of culture. The experiments showed that the cells treated with activin A increased quickly and grew faster than those in control group. Moreover, OVCAR-3 cells treated with activin A for 48 h proliferated significantly greater than those treated for 24 h or 72 h （P〈0.01）. bcl-2 protein expression increased expression in activin A treated group than in control group （P〈0.05）. Conclusion： Activin A could increase the proliferation of OVCAR-3 cells which may be through bcl-2 anti-apoptosis pathway.
文摘Objective:To investigate the interaction of p53 with docetaxel and berberine and their anticancer activities against oral squamous cell carcinoma.Methods:The interaction between p53 with docetaxel and berberine was investigated and their mechanisms of action against oral squamous cell carcinoma were studied.Toxicity studies were performed to determine any toxic impact of the drugs on the vital organs of tested animals.Results:In silico results revealed the molecular interaction of docetaxel and berberine with p53 and the molecules were found to be potential p53 inducers.Docetaxel and berberine inhibited the proliferation of cancer cells in a concentration-dependent manner.Flow cytometry analysis revealed that docetaxel and berberine at IC50 concentrations upregulated the expression of p53 in oral squamous cell carcinoma cells,thus triggering apoptotic cell death.In addition,no toxicity was observed in the liver and kidney tissues of mice after docetaxel and berberine treatment.Conclusions:Docetaxel and berberine significantly suppressed the proliferation of oral cancer cells by activating p53 expression and causing apoptotic cell death.Both compounds can be potential agents for the treatment of oral cancer,with little to no toxicity at the tissue level.
