黏液瘤病毒作用PI3K/AKT通路诱导子宫内膜癌细胞凋亡

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.

Myxoma virus induces apoptosis via PI3K/AKT pathway in endometrial cancer cells

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.