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目的:红系衍生的核因子2相关因子2(Nrf2)在蛋白酶体抑制剂硼替佐米诱导甲状腺癌细胞凋亡中的作用。方法:选取一系列人甲状腺未分化癌细胞系FRO、KTC1、KTC2、KTC3、8305C和8505C,分别设空白对照组和万珂处理组;蛋白质印迹法检测甲状腺癌细胞中Nrf2蛋白表达情况;共聚焦显微镜检测Nrf2甲状腺癌细胞核定位;流式细胞仪(FCM)检测细胞凋亡情况。结果:与FRO和KTC2细胞相比,Nrf2在人甲状腺癌细胞系8505C和8305C细胞中基础水平呈现高表达,万珂诱导后的表达增加更高,但对万珂诱导的细胞凋亡表现出不敏感,4种细胞的细胞凋亡率分别为(51.98±3.01)%、(46.92±2.72)%、(17.33±4.18)%和(7.97±1.01)%;万珂可诱导8505C和8305C细胞中的Nrf2细胞核易位。结论:Nrf2抑制蛋白酶体抑制剂诱导的甲状腺癌细胞凋亡,其抗凋亡作用可能源于蛋白酶体抑制剂诱导其细胞核转位。
Objective: The role of erythroid derived nuclear factor 2 related factor 2 (Nrf2) in the apoptosis of thyroid cancer cells induced by bortezomib, a proteasome inhibitor. Methods: A series of human thyroid undifferentiated carcinoma cell lines, FRO, KTC1, KTC2, KTC3, 8305C and 8505C, were randomly divided into blank control group and Velcade group. Western blotting was used to detect Nrf2 protein expression in thyroid carcinoma cells. The nuclear localization of Nrf2 in thyroid cancer cells was detected by microscopy and the apoptosis was detected by flow cytometry (FCM). Results: Compared with FRO and KTC2 cells, Nrf2 showed high basal levels in human thyroid carcinoma cell lines 8505C and 8305C, increased the expression of Velcro after induction, but showed no evidence of atoll-induced apoptosis (51.98 ± 3.01)%, (46.92 ± 2.72)%, (17.33 ± 4.18)%, and (7.97 ± 1.01)%, respectively. In addition, Velocity could induce apoptosis in 8505C and 8305C cells Nrf2 nuclear translocation. Conclusion: Nrf2 inhibits the apoptosis of thyroid carcinoma cells induced by proteasome inhibitor, and its anti-apoptotic effect may be due to the proteasome inhibitor inducing its nuclear translocation.