Objective The toxicology of TCDD （2,3,7,8-tetrachlorodibenzo-p-dioxin） has been studied mainly with regard to the carcinogenicity of its metabolites, but its phototoxicity is not well understood. Although some studi...Objective The toxicology of TCDD （2,3,7,8-tetrachlorodibenzo-p-dioxin） has been studied mainly with regard to the carcinogenicity of its metabolites, but its phototoxicity is not well understood. Although some studies have indicated the lethal phototoxicity of TCDD, this study was designed to investigate its effect on SPC-Al cells. Methods SPC-Al cells were cultured in 1640 medium and treated with 10 nmol/L, 0.1 μmol/L, 1 μmol/L TCDD for either 24 h or 96 h at each concentration. SPC-Al cells were co-cultured with TCDD at different concentrations. Then the cell morphology, DNA fragment electrophoresis, and cell cycle were analyzed by flow cytometry, and enzyme assays were used to observe the effect of TCDD on the morphology, growth rate, and enxyme change of SPC-A1 cells. Results With the increasing concentrations of TCDD and prolongation of culture time, the morphology of SPC-Alcells was changed from round shape to spindle, and the ability of SPC-Al cells to adhere to wall was decreased. With debris emitted around the cells, the morphologic changes included reduction in cell volume. Nuclear ehromatin condensation and PI were observed. With the increasing concentrations of TCDD, DNA ladder occurred. After treatment with TCDD, extraction of cancer cells exhibited typical DNA fragmentation, and flow eytometry analysis showed apoptosis in a dose-dependent manner. As the concentration of TCDD rose from 10 nmol/L to 1 μmol/L, the ratio of apoptotic cells increased from 10.76% to 21.82%. Conclusions TCDD has in vitro cytotoxicity on SPC-Al cells, and the cytotoxicity is positively related to its concentration and culture time. TCDD may inhibit the growth and proliferation of SPC-A lcells through the pathway of apoptosis introduction.展开更多
目的探讨miRNA-181c(miR-181c)在人肺腺癌组织中的表达及其对人肺腺癌细胞系SPC-A1增殖和侵袭的影响。方法收集37例肺腺癌患者组织标本,实时荧光定量PCR(qRT-PCR)检测肺腺癌组织及相应癌旁组织中miR-181c的表达水平。脂质体法将miR-181...目的探讨miRNA-181c(miR-181c)在人肺腺癌组织中的表达及其对人肺腺癌细胞系SPC-A1增殖和侵袭的影响。方法收集37例肺腺癌患者组织标本,实时荧光定量PCR(qRT-PCR)检测肺腺癌组织及相应癌旁组织中miR-181c的表达水平。脂质体法将miR-181c模拟物和miR-181c抑制剂分别转染至SPC-A1细胞中,CCK-8增殖实验检测转染后SPC-A1细胞的增殖能力,Transwell法检测转染后SPC-A1细胞的侵袭能力。结果肺腺癌组织中miR-181c的表达水平[3.259(1.637,4.920)×10-3]高于癌旁组织[2.008(1.200,3.292)×10-3],差异有统计学意义(U=-641.0,P<0.05)。miR-181c的表达水平与淋巴结转移密切相关(P<0.05)。转染SPC-A1细胞120 h后,miR-181c模拟物转染组的细胞增殖能力高于于阴性对照组,差异有统计学意义(2.029±0.034 vs 1.476±0.071;t=7.044,P<0.01);而miR-181c抑制剂转染组细胞的增殖能力弱于阴性对照组,差异有统计学意义(0.998±0.050 vs 1.414±0.058;t=5.461,P<0.01)。Transwell结果显示,转染miR-181c模拟物后SPC-A1侵袭能力显著增强(432.00±12.22 vs 219.50±9.31;t=14.11,P<0.01),转染抑制剂后侵袭能力显著减弱(73.60±5.32 vs 227.30±11.27;t=11.52,P<0.01)。结论 miR-181c在肺腺癌组织中高表达,并能促进SPC-A1细胞的增殖与侵袭。展开更多
基金This work was supported by the grant from National Natural Science Foundation of China (20275012).
文摘Objective The toxicology of TCDD （2,3,7,8-tetrachlorodibenzo-p-dioxin） has been studied mainly with regard to the carcinogenicity of its metabolites, but its phototoxicity is not well understood. Although some studies have indicated the lethal phototoxicity of TCDD, this study was designed to investigate its effect on SPC-Al cells. Methods SPC-Al cells were cultured in 1640 medium and treated with 10 nmol/L, 0.1 μmol/L, 1 μmol/L TCDD for either 24 h or 96 h at each concentration. SPC-Al cells were co-cultured with TCDD at different concentrations. Then the cell morphology, DNA fragment electrophoresis, and cell cycle were analyzed by flow cytometry, and enzyme assays were used to observe the effect of TCDD on the morphology, growth rate, and enxyme change of SPC-A1 cells. Results With the increasing concentrations of TCDD and prolongation of culture time, the morphology of SPC-Alcells was changed from round shape to spindle, and the ability of SPC-Al cells to adhere to wall was decreased. With debris emitted around the cells, the morphologic changes included reduction in cell volume. Nuclear ehromatin condensation and PI were observed. With the increasing concentrations of TCDD, DNA ladder occurred. After treatment with TCDD, extraction of cancer cells exhibited typical DNA fragmentation, and flow eytometry analysis showed apoptosis in a dose-dependent manner. As the concentration of TCDD rose from 10 nmol/L to 1 μmol/L, the ratio of apoptotic cells increased from 10.76% to 21.82%. Conclusions TCDD has in vitro cytotoxicity on SPC-Al cells, and the cytotoxicity is positively related to its concentration and culture time. TCDD may inhibit the growth and proliferation of SPC-A lcells through the pathway of apoptosis introduction.
文摘目的探讨miRNA-181c(miR-181c)在人肺腺癌组织中的表达及其对人肺腺癌细胞系SPC-A1增殖和侵袭的影响。方法收集37例肺腺癌患者组织标本,实时荧光定量PCR(qRT-PCR)检测肺腺癌组织及相应癌旁组织中miR-181c的表达水平。脂质体法将miR-181c模拟物和miR-181c抑制剂分别转染至SPC-A1细胞中,CCK-8增殖实验检测转染后SPC-A1细胞的增殖能力,Transwell法检测转染后SPC-A1细胞的侵袭能力。结果肺腺癌组织中miR-181c的表达水平[3.259(1.637,4.920)×10-3]高于癌旁组织[2.008(1.200,3.292)×10-3],差异有统计学意义(U=-641.0,P<0.05)。miR-181c的表达水平与淋巴结转移密切相关(P<0.05)。转染SPC-A1细胞120 h后,miR-181c模拟物转染组的细胞增殖能力高于于阴性对照组,差异有统计学意义(2.029±0.034 vs 1.476±0.071;t=7.044,P<0.01);而miR-181c抑制剂转染组细胞的增殖能力弱于阴性对照组,差异有统计学意义(0.998±0.050 vs 1.414±0.058;t=5.461,P<0.01)。Transwell结果显示,转染miR-181c模拟物后SPC-A1侵袭能力显著增强(432.00±12.22 vs 219.50±9.31;t=14.11,P<0.01),转染抑制剂后侵袭能力显著减弱(73.60±5.32 vs 227.30±11.27;t=11.52,P<0.01)。结论 miR-181c在肺腺癌组织中高表达,并能促进SPC-A1细胞的增殖与侵袭。
