信号转导和转录激活子5信号转导途径对受辐射KG-1细胞周期的调控作用

探讨信号转导和转录激活子５（ＳＴＡＴ５）信号转导途径在受辐射ＫＧ－１细胞中对细胞周期的调控作用。通过转染ＳＴＡＴ５基因的显性负突变体（ＤＮ－ＳＴＡＴ５）阻断ＪＡＫ／ＳＴＡＴ的信号传递后，瞬间转染ｃｙｃｌｉｎＤ１基因及ｃｙｃｌｉｎＢ１基因，观察ｃｙｃｌｉｎＤ１蛋白及ｃｙｃｌｉｎＢ１蛋白对受辐射细胞周期阻滞的影响作用。转染ＤＮ－ＳＴＳＡＴ５基因的受辐射ＫＧ－１细胞即使用粒－巨噬细胞集落刺激因子（ＧＭ－ＣＳＦ）刺激亦不能跳出Ｇ１期阻滞；瞬间转染ｃｙｃｌｉｎＤ１基因及ｃｙｃｌｉｎＢ１基因分别能促进受辐射细胞跳出Ｇ１期和Ｇ２期阻滞。ＧＭ－ＣＳ所激活的ＪＡＫ／ＳＴＡＴ信号转导途径通过促进周期蛋白ｃｙｃｌｉｎＤ１及ｃｙｃｌｉｎＢ１的表达而对受辐射细胞周期进行调控。

THE REGULATION EFFECT OF STAT5 SIGNALING PATHWAY ON THE CELLCYCLE PROGRESSION OF IRRADIATED KG-1 CELLS

This study investigated the role of the JAK/STAT signaling pathway regulating cell cycle progression in the irradiated KG-1 cells. By permanent transfecting the cells with DN-STAT5 cDNA to block the JAK/STAT signaling pathway and then transient transfecting with cyclin D1 or cyclin B1 cDNA, the effects of cyclin D1 protein and cyclin B1 protein on the cell cycle progression were examined. Results showed that after irradiation with 8Gy 60Co r rays, the irradiated KG-1 cells transfected with only DN-STAT5 cDNA can not recover form the G1 arrest, even though GM-CSF was added. Meanwhile, the cells transfected with both the DN-STAT5 cDNA and cyclin D1 cDNA or cyclin B1 cDNA can recover from the G1 arrest or the G2 arrest to a great extent. Thus, it was proved indirectly that the JAK/STAT signaling pathway activated by GM-CSF regulated the cell cycle progression through cyclin D1 and cyclin B1 protein.