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目的:探讨肿瘤坏死因子相关凋亡诱导配体(TRAIL)联合衣霉素促甲状腺未分化癌细胞系凋亡的作用机制。方法:通过TRAIL单用或联合衣霉素对多种甲状腺未分化癌细胞系进行作用,并以正常甲状腺上皮细胞系HTori-3作对照,采用蛋白印迹杂交法检测衣霉素处理前后各组细胞TRAIL死亡受体,诱杀受体和凋亡相关分子的蛋白表达水平。流式细胞术检测各组细胞凋亡状态。结果:与对照组相比,衣霉素作用后,肿瘤细胞死亡受体DR4、DR5和诱杀受体DcR1、DcR2表达无明显变化(P>0.05),而存活素水平明显降低,P<0.05。TRAIL与衣霉素单用对甲状腺癌细胞均无明显杀伤作用,最高凋亡细胞比率分别为10.68%和10.14%;衣霉素与TRAIL联合组凋亡细胞比率最大达60.5%;但在存活素过表达甲状腺未分化癌ARO细胞中,凋亡细胞比率降低50%左右。结论:在体外单用TRAIL对甲状腺癌细胞增殖无明显抑制作用,衣霉素明显增加肿瘤细胞对TRAIL敏感性,其增敏机制至少部分与下调存活素水平有关。
Objective: To investigate the mechanism of apoptosis associated with tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and tunicamycin-induced thyrotropin undifferentiated carcinoma cell line. Methods: A variety of thyroid undifferentiated carcinoma cell lines were treated with TRAIL alone or in combination with tunicamycin. The normal thyroid epithelial cell line HTori-3 was used as a control. Western blotting was used to detect the expression of all the cytokines TRAIL death receptor, decoy receptor and apoptosis related protein expression levels. Cell apoptosis was detected by flow cytometry. Results: Compared with the control group, there was no significant change in the expression of DR4, DR5 and DcR1, DcR2, but survivin in tunicamycin group (P <0.05). TRAIL and tunicamycin alone had no significant killing effect on thyroid cancer cells, the highest apoptotic cells were 10.68% and 10.14% respectively; the ratio of apoptotic cells in tunicamycin and TRAIL group was up to 60.5% Overexpression of thyroid undifferentiated ARO cells, apoptotic cells decreased by about 50%. CONCLUSION: TRAIL alone has no inhibitory effect on the proliferation of thyroid carcinoma cells in vitro. Tunicamycin can significantly increase the sensitivity of tumor cells to TRAIL. The mechanism of sensitization to TRAIL is at least partly related to the down-regulation of the level of survivin.