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目的 :探讨IL 6对急性髓系白血病 (AML)细胞产生生物学效应的信号转导基础。方法 :测定IL 6对M1,R2 ,K5 6 2 ,TF1细胞生长的影响 ,并采用凝胶阻滞电泳 (Electrophoresismobilityshiftassay ,EMSA)的方法分析IL 6对这些AML细胞信号转导子与转录激活子 3(Signaltransducerandactivatoroftranscription 3 ,STAT3)与核因子介素 6 (nuclearfactor IL6 ,NF IL6 )的激活情况。在此基础上 ,运用STAT3、NF IL6反义寡核苷酸 (ASODNs)阻断或减弱IL 6在M1细胞中对STAT3与NF IL6的激活 ,检测ASODNs对IL 6诱导的M1细胞生长停止效应的影响。结果 :NF IL6在所有AML细胞中均有组成型激活 ,而STAT3仅在R2、K5 6 2细胞中有弱的组成型激活。STAT3ASODN可部分拮抗IL 6对M1细胞的抑制 ,而NF IL6ASODN可加强IL 6对M1细胞的抑制。结论 :STAT3在AML细胞中可能负调控细胞生长 ,而NF IL6很可能与细胞生存、增殖有关
Objective: To explore the basis of signal transduction of IL 6 on the biological effects of acute myeloid leukemia (AML) cells. METHODS: The effects of IL 6 on the growth of M1, R2, K562, and TF1 cells were measured, and signal transduction and transcriptional activators of IL-6 were analyzed by electrophoresis mobility shift assay (EMSA). (Signal transducer and activator of transcription 3 , STAT3) and activation of nuclear factor IL6 (NF IL6). On this basis, STAT3 and NF-IL6 antisense oligonucleotides (ASODNs) were used to block or attenuate the activation of STAT3 and NF-IL6 by IL-6 in M1 cells, and to detect the effect of ASODNs on IL-6-induced M1 cell growth arrest. influences. RESULTS: NF-IL6 was constitutively activated in all AML cells, whereas STAT3 was only weakly constitutively activated in R2 and K562 cells. STAT3ASODN partially antagonized the inhibition of M6 cells by IL-6, while NF IL6ASODN enhanced IL-6 inhibition of M1 cells. Conclusion: STAT3 may negatively regulate cell growth in AML cells, and NF-IL6 is probably related to cell survival and proliferation.