浙江医学
浙江醫學
절강의학
ZHEJIANG MEDICAL JOURNAL
2013年
19期
1736-1738,1772
,共4页
肝癌%糖原合成激酶- 3%氯化锂%CyclinD1
肝癌%糖原閤成激酶- 3%氯化鋰%CyclinD1
간암%당원합성격매- 3%록화리%CyclinD1
Liver cancer%Glycogen synthase kinase 3%Lithium chloride%CyclinD1
目的:探讨氯化锂对人肝癌细胞BEL-7402增殖、周期的影响及其作用机制。方法应用MTT法及DNA PREP细胞周期法检测BEL-7402经氯化锂作用后的增殖及周期改变情况,Western blot检测糖原合成激酶-3(GSK-3)、失活pGSK-3及其下游分子CyclinD1的表达情况。结果氯化锂可显著抑制BEL-7402的增殖,并呈时间、剂量依赖性(P<0.05);氯化锂可使BEL-7402的G0/G1期比例明显降低、G2/M期比例显著升高(P<0.05);氯化锂作用后GSK-3、失活pGSK-3及CyclinD1蛋白的表达水平均明显升高(P<0.05)。结论氯化锂可抑制肝癌细胞增殖,其机制可能是通过抑制GSK-3活性并上调CyclinD1表达使肝癌细胞阻滞于G2/M期。
目的:探討氯化鋰對人肝癌細胞BEL-7402增殖、週期的影響及其作用機製。方法應用MTT法及DNA PREP細胞週期法檢測BEL-7402經氯化鋰作用後的增殖及週期改變情況,Western blot檢測糖原閤成激酶-3(GSK-3)、失活pGSK-3及其下遊分子CyclinD1的錶達情況。結果氯化鋰可顯著抑製BEL-7402的增殖,併呈時間、劑量依賴性(P<0.05);氯化鋰可使BEL-7402的G0/G1期比例明顯降低、G2/M期比例顯著升高(P<0.05);氯化鋰作用後GSK-3、失活pGSK-3及CyclinD1蛋白的錶達水平均明顯升高(P<0.05)。結論氯化鋰可抑製肝癌細胞增殖,其機製可能是通過抑製GSK-3活性併上調CyclinD1錶達使肝癌細胞阻滯于G2/M期。
목적:탐토록화리대인간암세포BEL-7402증식、주기적영향급기작용궤제。방법응용MTT법급DNA PREP세포주기법검측BEL-7402경록화리작용후적증식급주기개변정황,Western blot검측당원합성격매-3(GSK-3)、실활pGSK-3급기하유분자CyclinD1적표체정황。결과록화리가현저억제BEL-7402적증식,병정시간、제량의뢰성(P<0.05);록화리가사BEL-7402적G0/G1기비례명현강저、G2/M기비례현저승고(P<0.05);록화리작용후GSK-3、실활pGSK-3급CyclinD1단백적표체수평균명현승고(P<0.05)。결론록화리가억제간암세포증식,기궤제가능시통과억제GSK-3활성병상조CyclinD1표체사간암세포조체우G2/M기。
Objective To investigate the effect of lithium chloride (LiCl) on cellproliferation,cellcycle of human hepatoma cells and its mechanism. Methods Cultured human hepatoma BEL- 7402 cells were treated with different concentrations of LiCl. cellproliferation was measured by MTT assay and cellcycle was examined by DNA PREP cell cycle assay. The expressions of GSK- 3, inactivated GSK- 3 and CyclinD1 were determined by Western blot. Results LiCl inhibited BEL- 7402 cellproliferation in a concentration- and time- dependent manner. After LiCl treatment the percentage of G0/G1 phase was significantly reduced, the G2/M phase was significantly increased, and the expression levels of GSK- 3, inactivated GSK- 3 and CyclinD1 were up- regulat-ed. Conclusion LiCl can inhibit the proliferation of BEL- 7402 cells, in which inactivation of GSK- 3 and up- regulation of CyclinD1 may be involved leading to cellcycle arrest in G2/M phase.