南方医科大学学报
南方醫科大學學報
남방의과대학학보
JOURNAL OF SOUTHERN MEDICAL UNIVERSITY
2013年
9期
1304-1307
,共4页
张媛媛%刘哲%张倩雯%晁振华%张配%夏飞%蒋琛琛%刘浩%蒋志文
張媛媛%劉哲%張倩雯%晁振華%張配%夏飛%蔣琛琛%劉浩%蔣誌文
장원원%류철%장천문%조진화%장배%하비%장침침%류호%장지문
乳腺癌细胞%3-溴丙酮酸%糖酵解%ATP%活性氧
乳腺癌細胞%3-溴丙酮痠%糖酵解%ATP%活性氧
유선암세포%3-추병동산%당효해%ATP%활성양
breast cancer cells%3-bromopyruvate%glycolysis%ATP%reactive oxygen
目的探讨糖酵解抑制剂3-溴丙酮酸(3-BrPA)诱导乳腺癌细胞SK-BR-3凋亡的作用及其可能相关机制。方法MTT法检测3-BrPA对乳腺癌细胞SK-BR-3增殖的抑制作用;碘化丙啶(PI)单染流式细胞术检测细胞凋亡;ATP检测试剂盒检测细胞内ATP水平;DHE荧光探针标记法检测细胞内超氧阴离子水平;线粒体膜电位检测试剂盒(JC-1)检测细胞线粒体膜电位。结果MTT结果显示,3-BrPA可抑制SK-BR-3细胞的增殖活性,且呈浓度和时间依赖性。80、160、320μmol·L-1的3-BrPA诱导SK-BR-3细胞24 h的凋亡率分别为6.7%、22.3%、79.6%。80、160、320μmol·L-13-BrPA作用于SK-BR-3细胞5 h后,细胞内ATP水平与对照组相比分别为87.7%、60.6%、23.7%。160μmol·L-1的3-BrPA增加SK-BR-3细胞中活性氧的生成,同时使细胞线粒体膜电位降低。结论3-BrPA可以抑制乳腺癌细胞SK-BR-3的增殖活性,引起线粒体膜电位降低,并且诱导其凋亡,机制可能与抑制肿瘤细胞的糖酵解从而减少ATP的产生并升高细胞内活性氧的水平有关。
目的探討糖酵解抑製劑3-溴丙酮痠(3-BrPA)誘導乳腺癌細胞SK-BR-3凋亡的作用及其可能相關機製。方法MTT法檢測3-BrPA對乳腺癌細胞SK-BR-3增殖的抑製作用;碘化丙啶(PI)單染流式細胞術檢測細胞凋亡;ATP檢測試劑盒檢測細胞內ATP水平;DHE熒光探針標記法檢測細胞內超氧陰離子水平;線粒體膜電位檢測試劑盒(JC-1)檢測細胞線粒體膜電位。結果MTT結果顯示,3-BrPA可抑製SK-BR-3細胞的增殖活性,且呈濃度和時間依賴性。80、160、320μmol·L-1的3-BrPA誘導SK-BR-3細胞24 h的凋亡率分彆為6.7%、22.3%、79.6%。80、160、320μmol·L-13-BrPA作用于SK-BR-3細胞5 h後,細胞內ATP水平與對照組相比分彆為87.7%、60.6%、23.7%。160μmol·L-1的3-BrPA增加SK-BR-3細胞中活性氧的生成,同時使細胞線粒體膜電位降低。結論3-BrPA可以抑製乳腺癌細胞SK-BR-3的增殖活性,引起線粒體膜電位降低,併且誘導其凋亡,機製可能與抑製腫瘤細胞的糖酵解從而減少ATP的產生併升高細胞內活性氧的水平有關。
목적탐토당효해억제제3-추병동산(3-BrPA)유도유선암세포SK-BR-3조망적작용급기가능상관궤제。방법MTT법검측3-BrPA대유선암세포SK-BR-3증식적억제작용;전화병정(PI)단염류식세포술검측세포조망;ATP검측시제합검측세포내ATP수평;DHE형광탐침표기법검측세포내초양음리자수평;선립체막전위검측시제합(JC-1)검측세포선립체막전위。결과MTT결과현시,3-BrPA가억제SK-BR-3세포적증식활성,차정농도화시간의뢰성。80、160、320μmol·L-1적3-BrPA유도SK-BR-3세포24 h적조망솔분별위6.7%、22.3%、79.6%。80、160、320μmol·L-13-BrPA작용우SK-BR-3세포5 h후,세포내ATP수평여대조조상비분별위87.7%、60.6%、23.7%。160μmol·L-1적3-BrPA증가SK-BR-3세포중활성양적생성,동시사세포선립체막전위강저。결론3-BrPA가이억제유선암세포SK-BR-3적증식활성,인기선립체막전위강저,병차유도기조망,궤제가능여억제종류세포적당효해종이감소ATP적산생병승고세포내활성양적수평유관。
Objective To study the effect of glycolysis inhibitor 3-bromopyruvate (3-BrPA) in inducing apoptosis of human breast carcinoma cells SK-BR-3 and the possible mechanism. Methods MTT assay was used to detect the growth inhibition induced by 3-BrPA in breast cancer cells SK-BR-3. The apoptotic cells were detected by flow cytometry with propidium iodide (PI). ATP levels in the cells were detected by ATP assay kit, and DHE fluorescent probe technique was used to determine superoxide anion levels; the mitochondrial membrane potential was assessed using JC-1 staining assay. Results MTT assay showed that the proliferation of SK-BR-3 cells was inhibited by 3-BrPA in a time- and concentration-dependent manner. Exposure to 80, 160, and 320μmol·L-1 3-BrPA for 24 h resulted in cell apoptosis rates of 6.7%, 22.3%, and 79.6%, respectively, and the intracellular ATP levels of SK-BR-3 cells treated with 80, 160, 320μmol·L-1 3-BrPA for 5 h were 87.7%, 60.6%, and 23.7%of the control levels. 3-BrPA at 160μmol·L-1 increased reactive oxygen levels and lowered mitochondrial membrane potential of SK-BR-3 cells. Conclusion 3-BrPA can inhibit cell proliferation, reduce the mitochondrial membrane potential and induce apoptosis in SK-BR-3 cells, the mechanism of which may involve a reduced ATP level by inhibiting glycolysis and increasing the reactive oxygen level in the cells.