以鼠腹腔微环境研究三氧化二砷对食管癌EC109细胞骨架的影响

目的:细胞骨架微丝是与肿瘤细胞生长密切相关的因素之一,本文以生物机体腹腔为免疫的微环境,研究化疗药物三氧化二砷(As2O3)对人食管癌细胞株微丝骨架的影响.方法:利用鬼笔环肽(Phalloidin)及碘化丙碇(Propidium Iodide,PI)标记,以流式细胞仪技术分析小鼠腹腔液中食管癌EC109细胞周期的各期细胞内F-actin的变化.结果:诱导肥大细胞(mast cell,MC)迁移入腹腔的同时,迅速升高G0/G1期细胞及降低S期细胞内的F-actin含量,DNA检测结果显示G0/G1期的肿瘤细胞数量迅速增加(p<0.05),S期细胞含量降低;三氧化二砷作用后,食管癌细胞各期的F-actin含量均降低,尤其S期为甚.MC和As2O3共同作用后,食管癌细胞各期的F-actin含量均也减少,但G0/G1期细胞数量却显著增加.结论:在小鼠腹腔微环境中,免疫功能改变(免疫细胞MC的聚集)引起G0/G1期细胞数量迅速升高、S期细胞的数量降低,可能促使EC109细胞G0/G1期向S期跨越的延迟;在此环境中,As2O3也可能通过抑制S期EC109细胞内F-actin的重组来延迟细胞从G0/G1期进入S期;诱导肥大细胞迁入腹腔的同时加入药物As2O3,其作用主要表现为短期效应,促进了肿瘤细胞内F-actin含量的降低,G0/G1期细胞数量较高,出现短暂的延迟G0/G1期向S期跨越,增强了对肿瘤细胞生长的抑制作用.因此,以生物机体为研究环境,可能更真实地呈现化疗药物对肿瘤细胞的治疗效果.

Effects of Arsenic Trioxide on Cytoskeleton of Esophageal Carcinoma EC109 Cells in Mouse Peritoneal Microenvironment

Objective： The microfilament cytoskeleton is one of the factors closely related with the growth of tumor cells. This paper aimed at establishing an immune mieroenvironment in living organisms abdominal, investigating the effects of chemotherapy drug arsenic trioxide （As2O3） on the F-actin cytoskeleton of human esophageal carcinoma EC109 cell line. Method： The cellular F-actin of EC109 cells were labeled with Phalloidin-FITC, DNA in esophageal carcinoma cells were labeled with propidium iodide（PI）. The F-actin content in each phase of cancer cell cycle was analyzed by flow cytometry. Results： Mast cell （MC） migrated into the abdominal cavity by induction could increase F-actin content in the G0/G1 phase cells but reduce in S phase. DNA test results showed that MC made the number of tumor cells in G0/G1 phase increase rapidly, while decrease in S phase. As203 reduced F-aetin content of esophageal carcinoma EC109 ceils, especially the F- actin content of S phase cells. With the effects of MC and As2O3, the F-actin content in each phase of EC109 cell cycle was decreased, but a significant increase in the number of cells in G0/G1 phase. Conclusions： In the mouse peritoneal microenvironment, when the immune function changed （this referred to the aggregation of MC）, it increased the number of tumor cells in G0/G1 phase rapidly, while decreased in S phase, so it could promote cell cycle G0/G1 phase across into S phase delay. As203 also could delay cells from G0/G1 phase into S phase by inhibition the F-actin reorganization of EC109 cells in S phase. We induced mast cell into the mouse peritoneal, at the same time adding drugs As2O3, and found that its role mainly as a short-term effect, reduced the F-actin content of tumour cell, but a higher number of cells in G0/G1 phase, and might promote a brief delay in the Go/Gt phase to S phase across. Therefore, the research system was in the biological body, this may more realistically show the therapeutic effect of the chemotherapeutic drugs on tumor cells.