中华实验和临床病毒学杂志
中華實驗和臨床病毒學雜誌
중화실험화림상병독학잡지
CHINESE JOURNAL OF EXPERIMENTAL AND CLINICAL VIROLOGY
2014年
4期
271-273
,共3页
周芸%许可可%郭蓉%黄敏%孙红杰
週蕓%許可可%郭蓉%黃敏%孫紅傑
주예%허가가%곽용%황민%손홍걸
子宫内膜肿瘤%细胞凋亡%黏液瘤病毒%体外研究
子宮內膜腫瘤%細胞凋亡%黏液瘤病毒%體外研究
자궁내막종류%세포조망%점액류병독%체외연구
Endometrial neoplasms%Apoptosis%Myxoma virus%in vitro
目的 探讨黏液瘤病毒(MV)对子宫内膜癌HEC-IB细胞凋亡和增殖的作用.方法 通过荧光染色等观察细胞核固缩和染色体碎片等形态学变化,MTT法测定MV对HEC-IB细胞的生长抑制作用,采用流式细胞仪和免疫印迹实验检测HEC-IB细胞的生长凋亡情况及其相关蛋白的表达变化.结果 MV对子宫内膜癌HEC-IB细胞具有明显的生长抑制作用,并能诱导细胞发生凋亡,随着作用时间的延长,细胞的生长抑制率及细胞凋亡率均明显升高.MV抑制细胞生长及诱导细胞发生凋亡的过程中,细胞磷脂酰肌醇-3激酶(PI3K)、蛋白激酶B(AKT)、糖原合酶激酶3(GSK3)表达水平及活性显著降低.结论 MV能够通过多条信号途径促进人子宫内膜癌HEC-IB细胞发生凋亡,通过抑制PI3K/AKT的活性是其体外诱导人子宫内膜癌HEC-IB细胞发生凋亡和抑制增值的重要作用机制.
目的 探討黏液瘤病毒(MV)對子宮內膜癌HEC-IB細胞凋亡和增殖的作用.方法 通過熒光染色等觀察細胞覈固縮和染色體碎片等形態學變化,MTT法測定MV對HEC-IB細胞的生長抑製作用,採用流式細胞儀和免疫印跡實驗檢測HEC-IB細胞的生長凋亡情況及其相關蛋白的錶達變化.結果 MV對子宮內膜癌HEC-IB細胞具有明顯的生長抑製作用,併能誘導細胞髮生凋亡,隨著作用時間的延長,細胞的生長抑製率及細胞凋亡率均明顯升高.MV抑製細胞生長及誘導細胞髮生凋亡的過程中,細胞燐脂酰肌醇-3激酶(PI3K)、蛋白激酶B(AKT)、糖原閤酶激酶3(GSK3)錶達水平及活性顯著降低.結論 MV能夠通過多條信號途徑促進人子宮內膜癌HEC-IB細胞髮生凋亡,通過抑製PI3K/AKT的活性是其體外誘導人子宮內膜癌HEC-IB細胞髮生凋亡和抑製增值的重要作用機製.
목적 탐토점액류병독(MV)대자궁내막암HEC-IB세포조망화증식적작용.방법 통과형광염색등관찰세포핵고축화염색체쇄편등형태학변화,MTT법측정MV대HEC-IB세포적생장억제작용,채용류식세포의화면역인적실험검측HEC-IB세포적생장조망정황급기상관단백적표체변화.결과 MV대자궁내막암HEC-IB세포구유명현적생장억제작용,병능유도세포발생조망,수착작용시간적연장,세포적생장억제솔급세포조망솔균명현승고.MV억제세포생장급유도세포발생조망적과정중,세포린지선기순-3격매(PI3K)、단백격매B(AKT)、당원합매격매3(GSK3)표체수평급활성현저강저.결론 MV능구통과다조신호도경촉진인자궁내막암HEC-IB세포발생조망,통과억제PI3K/AKT적활성시기체외유도인자궁내막암HEC-IB세포발생조망화억제증치적중요작용궤제.
Objective To investigate the apoptosis-inducing effect of myxoma virus in the human endometrial cancer HEC-IB cell line.Method A morphological analysis,nuclear condensation,and fragmentation of chromatin were monitored using immunofluorescence staining.Cell viability was assessed using MTT assay.Cell apoptosis and the apoptosis-related activation in the HEC-IB cell line were evaluated by flow cytometry and Western blotting,Result Suppressed the proliferation of the HEC-IB cell line in a time-dependent manner.The obvious inhibiting effect of MV on HEC-IB cells viability and its apoptosisinducing effect were observed.MV treatment downregulated the activation of protein kinase B (AKT) and the expression of glycogen synthase kinase 3 (GSK3),Conclusion MV induced apoptosis involved several molecular pathways.It may suppress constitutively activated targets of phoaphatidylinositol-3-kinases (PI3K) and AKT in the HEC-IB cell line,inhibiting the proliferation and induction of apoptosis.