AIM:To investigate the events associated with the apoptotic effect of p-Coumaric acid,one of the phenolic components of honey,in human colorectal carcinoma(HCT-15)cells.METHODS:3-(4,5-dimethylthiazol-2-yl)-2,5-dipheny...AIM:To investigate the events associated with the apoptotic effect of p-Coumaric acid,one of the phenolic components of honey,in human colorectal carcinoma(HCT-15)cells.METHODS:3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltertazolium-bromide assay was performed to determine the antiproliferative effect of p-Coumaric acid against colon cancer cells.Colony forming assay was conducted to quantify the colony inhibition in HCT15 and HT 29 colon cancer cells after p-Coumaric acid treatment.Propidium Iodide staining of the HCT15 cells using flow cytometry was done to study the changes in the cell cycle of treated cells.Identification of apoptosis was done using scanning electron microscope and photomicrograph evaluation of HCT 15cells after exposing to p-Coumaric acid.Levels of reactive oxygen species(ROS)of HCT 15 cells exposed to p-Coumaric acid was evaluated using 2’,7’-dichlorfluorescein-diacetate.Mitochondrial membrane potential of HCT-15 was assessed using rhodamine-123 with the help of flow cytometry.Lipid layer breaks associated with p-Coumaric acid treatment was quantified using the dye merocyanine 540.Apoptosis was confirmed and quantified using flow cytometric analysis of HCT15 cells subjected to p-Coumaric acid treatment after staining with YO-PRO-1.RESULTS:Antiproliferative test showed p-Coumaric acid has an inhibitory effect on HCT 15 and HT 29 cells with an IC50(concentration for 50%inhibition)value of 1400 and 1600μmol/L respectively.Colony forming assay revealed the time-dependent inhibition of HCT 15 and HT 29 cells subjected to p-Coumaric acid treatment.Propidium iodide staining of treated HCT 15cells showed increasing accumulation of apoptotic cells(37.45±1.98 vs 1.07±1.01)at sub-G1phase of the cell cycle after p-Coumaric acid treatment.HCT-15 cells observed with photomicrograph and scanning electron microscope showed the signs of apoptosis like blebbing and shrinkage after p-Coumaric acid exposure.Evaluation of the lipid layer showed increasing lipid layer breaks was associated with the growth inhibition of p-Coumaric acid.A fall in mitochondrial membrane potential and increasing ROS generation was observed in the p-Coumaric acid treated cells.Further apoptosis evaluated by YO-PRO-1 staining also showed the timedependent increase of apoptotic cells after treatment.CONCLUSION:These results depicted that p-Coumaric acid inhibited the growth of colon cancer cells by inducing apoptosis through ROS-mitochondrial pathway.展开更多
目的:研究微小RNA(microRNA,miR)-218-5p靶向调控三磷酸腺苷结合盒超家族G家族第2个成员(ATP-binding cassette sub-family G member 2,ABCG2)基因对Tca-8113细胞的增殖、迁移和侵袭的影响,并探讨其机制。方法:运用实时荧光定量聚合酶...目的:研究微小RNA(microRNA,miR)-218-5p靶向调控三磷酸腺苷结合盒超家族G家族第2个成员(ATP-binding cassette sub-family G member 2,ABCG2)基因对Tca-8113细胞的增殖、迁移和侵袭的影响,并探讨其机制。方法:运用实时荧光定量聚合酶链反应(quantitative Real-time PCR,qRT-PCR)与Western blot检测Tca-8113细胞和NOK细胞中miR-218-5p和ABCG2的表达。通过双荧光素酶报告基因实验检测miR-218-5p和ABCG2靶向关系。用脂质体法将miR-218-5p mimic、ABCG2小干扰RNA(interfering RNA,siRNA)、miR-218-5p mimic+pcDNA-ABCG2分别转染至Tca-8113细胞中,噻唑蓝(methyl thiazol tetrazolium,MTT)法、Transwell法检测Tca-8113细胞的增殖、迁移和侵袭。结果:与NOK细胞比较,Tca-8113细胞miR-218-5p呈显著低表达,ABCG2呈显著高表达(P<0.05)。过表达miR-218-5p、抑制ABCG2均可抑制Tca-8113细胞的增殖和迁移(P<0.05)。双荧光素酶报告基因实验证实miR-218-5p与ABCG2的靶向结合关系。过表达ABCG2可逆转上调miR-218-5p对Tca-8113细胞增殖、迁移和侵袭的抑制作用。结论:上调miR-218-5p的表达可靶向调控ABCG2,抑制Tca-8113细胞的增殖、迁移和侵袭,将可为口腔鳞状细胞癌的治疗提供新的靶点。展开更多
文章分析了M A S建模方法学提出的动因,指出了M A S建模中的关键问题;阐述了基于A gen t的建模方法学分析阶段的过程及其不足,研究了对系统子目标进行表述、求解的规范化工具——G/A矩阵及其求解方法;并在此基础上提出了一种新的M A S...文章分析了M A S建模方法学提出的动因,指出了M A S建模中的关键问题;阐述了基于A gen t的建模方法学分析阶段的过程及其不足,研究了对系统子目标进行表述、求解的规范化工具——G/A矩阵及其求解方法;并在此基础上提出了一种新的M A S中个体A gen t的识别方法,最后通过实例说明该方法简单易行。展开更多
基金Supported by Universiti Teknologi Malaysia,Malaysia for providing Visiting Research Fellowship
文摘AIM:To investigate the events associated with the apoptotic effect of p-Coumaric acid,one of the phenolic components of honey,in human colorectal carcinoma(HCT-15)cells.METHODS:3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltertazolium-bromide assay was performed to determine the antiproliferative effect of p-Coumaric acid against colon cancer cells.Colony forming assay was conducted to quantify the colony inhibition in HCT15 and HT 29 colon cancer cells after p-Coumaric acid treatment.Propidium Iodide staining of the HCT15 cells using flow cytometry was done to study the changes in the cell cycle of treated cells.Identification of apoptosis was done using scanning electron microscope and photomicrograph evaluation of HCT 15cells after exposing to p-Coumaric acid.Levels of reactive oxygen species(ROS)of HCT 15 cells exposed to p-Coumaric acid was evaluated using 2’,7’-dichlorfluorescein-diacetate.Mitochondrial membrane potential of HCT-15 was assessed using rhodamine-123 with the help of flow cytometry.Lipid layer breaks associated with p-Coumaric acid treatment was quantified using the dye merocyanine 540.Apoptosis was confirmed and quantified using flow cytometric analysis of HCT15 cells subjected to p-Coumaric acid treatment after staining with YO-PRO-1.RESULTS:Antiproliferative test showed p-Coumaric acid has an inhibitory effect on HCT 15 and HT 29 cells with an IC50(concentration for 50%inhibition)value of 1400 and 1600μmol/L respectively.Colony forming assay revealed the time-dependent inhibition of HCT 15 and HT 29 cells subjected to p-Coumaric acid treatment.Propidium iodide staining of treated HCT 15cells showed increasing accumulation of apoptotic cells(37.45±1.98 vs 1.07±1.01)at sub-G1phase of the cell cycle after p-Coumaric acid treatment.HCT-15 cells observed with photomicrograph and scanning electron microscope showed the signs of apoptosis like blebbing and shrinkage after p-Coumaric acid exposure.Evaluation of the lipid layer showed increasing lipid layer breaks was associated with the growth inhibition of p-Coumaric acid.A fall in mitochondrial membrane potential and increasing ROS generation was observed in the p-Coumaric acid treated cells.Further apoptosis evaluated by YO-PRO-1 staining also showed the timedependent increase of apoptotic cells after treatment.CONCLUSION:These results depicted that p-Coumaric acid inhibited the growth of colon cancer cells by inducing apoptosis through ROS-mitochondrial pathway.
文摘文章分析了M A S建模方法学提出的动因,指出了M A S建模中的关键问题;阐述了基于A gen t的建模方法学分析阶段的过程及其不足,研究了对系统子目标进行表述、求解的规范化工具——G/A矩阵及其求解方法;并在此基础上提出了一种新的M A S中个体A gen t的识别方法,最后通过实例说明该方法简单易行。
