为了观察P44/42 MAPK和STAT3在γ射线诱发的小鼠白血病骨髓细胞中的变化情况,首先利用γ射线诱发Balb/C小鼠发生白血病,成功地建立了辐射致癌模型.在此基础上,将动物分为三组:癌变组、辐射未癌变组和对照组,利用免疫沉淀和免疫印迹技术,检测各组骨髓细胞的P44/42 MAPK和STAT3蛋白及磷酸化水平变化情况.结果显示:癌变组骨髓细胞P44/42 MAPK蛋白及磷酸化水平均高于辐射未癌变组和对照组(P<0.05);而STAT3蛋白及磷酸化水平在三组骨髓细胞之间无显著差异(P>0.05).说明Ras/ P44/42 MAPK途径可能在γ射线诱发的小鼠白血病中发挥一定的作用,而JAK/STAT3途径并未参与这一癌变过程.
In order to study the possible role of the p44/42 mitogenactivated protein kinases(MAPK) and the signal transducer and activator of transcription 3 (STAT3) in the cancerization process of leukemia marrow cell induced by γ-ray irradiation, the mice were divided into three groups according to the pathological examination: the carcinomatous group, the uncarcinomatous control group and the unirradiated control group. The level of phospho-STAT3 were detected by the immunoprecipitation and Western blotting assay, and the change of the expression of the P44/42 MAPK, phospho-P44/42 MAPK and STAT3 were detected by Western blotting analysis. The results showed that the levels of P44/42 MAPK and phospho-P44/42 MAPK were significantly higher in the marrow cell of the carcinomatous group than that in the control groups (P<0.05) respectively. But statistically, there was no difference in the levels of STAT3 and phospho-STAT3 among the three groups (P>0.05). All the results suggest that there is a possible involvement of Ras/ P44/42 MAPK pathways in the cancerization process of leukemia cell, while JAK/STAT3 pathway makes no contribution to the process of radiation carcinogenesis.
傅志超,蔡建明,韩玲,王凤玫,黄定德,黄越承,李百龙,高建国. P44/42 MAPK和STAT3在γ射线诱发的小鼠白血病骨髓细胞中的表达[J].生物化学与生物物理进展,2003,30(2):199-203
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