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目的:研究莱菔硫烷(SFN)对头颈癌细胞系PCI-13中信号转导和转录激活因子1和3(STAT1,STAT3)的影响,探讨STAT/JAK途径在SFN抗肿瘤中的作用。方法:体外培养PCI-13细胞,经血清饥饿后,分别用0、10、20、40μmol/L的SFN处理3、6、12、24 h。为检测IL-6诱导的STAT3激活情况,用20、40μmol/L的SFN处理24 h,再用50 ng/ml的IL-6处理15min。设阴性和阳性对照组。分别获取细胞后,采用流式细胞术检测磷酸化-STAT(p-STAT)1和3的表达。结果:SFN对pSTAT1表达无影响,但可以显著抑制p-STAT3的表达,还可以抑制IL-6诱导的p-STAT3的升高,这种抑制存在浓度和时间依赖性。结论:SFN能够抑制PCI-13细胞中的STAT3的磷酸化水平,减少其构成性激活和IL-6诱导的激活,提示SFN诱导PCI-13细胞凋亡可能由STAT/JAK途径介导。
Objective: To investigate the effects of sulforaphane (SFN) on signal transducers and activators of transcription 1 and 3 (STAT1, STAT3) in human head and neck cancer cell line PCI-13 and to explore the role of STAT / JAK pathway in antitumor of SFN. Methods: PCI-13 cells were cultured in vitro and were treated with 0, 10, 20 and 40 μmol / L SFN for 3, 6, 12 and 24 h after serum starvation. To detect IL-6-induced activation of STAT3, SF40 treated with 20 and 40 μmol / L of SFN for 24 h followed by 50 ng / ml of IL-6 for 15 min. Set negative and positive control group. After obtaining the cells respectively, the expression of phospho-STAT (p-STAT) 1 and 3 was detected by flow cytometry. Results: SFN had no effect on the expression of pSTAT1, but significantly inhibited the expression of p-STAT3, and also inhibited the increase of p-STAT3 induced by IL-6. The inhibition was concentration-dependent and time-dependent. Conclusion: SFN can inhibit the phosphorylation of STAT3 in PCI-13 cells and decrease its constitutive activation and IL-6-induced activation, suggesting that SFN-induced apoptosis of PCI-13 cells may be mediated by the STAT / JAK pathway.