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目的：本研究从细胞周期调控这一角度来探讨视黄酸类物质阻遏白血病细胞增殖的分子机理。方法：采用两步过量胸苷阻断法将ＨＬ－６０细胞同步化于Ｇ１／Ｓ期边缘，５×１０－６ｍｏｌ／Ｌ视黄酸或芳维甲处理１ｄ～４ｄ后收获细胞，以流式细胞仪（ＦＣＭ）分析细胞周期相分布，免疫印迹法检测ＣｙｃｌｉｎＥ、ＣｙｃｌｉｎＤ１和Ｐ３４ｃｄｋ２蛋白表达水平。结果：ＣｙｃｌｉｎＥ和Ｄ１蛋白表达量具有周期依赖性，Ｇ１期开始增加，Ｓ期达到高峰，Ｇ２期逐渐下降，而Ｐ３４ｃｄｋ２蛋白表达量在整个细胞周期中无明显变化；视黄酸或芳维甲处理后，大部分细胞被阻断在Ｇ０／Ｇ１期，Ｐ３４ｃｄｋ２蛋白表达量变化不明显，而ＣｙｃｌｉｎＥ和Ｄ１蛋白表达量明显下降。结论：视黄酸或芳维甲诱导的ＣｙｃｌｉｎＥ和ＣｙｃｌｉｎＤ１蛋白表达的降低，可能与视黄酸类物质干扰细胞Ｇ１→Ｓ期转换、阻遏ＨＬ－６０细胞增殖并诱导其分化有关。
OBJECTIVE: This study explored the molecular mechanism by which retinoids inhibit the proliferation of leukemia cells from the perspective of cell cycle regulation. Methods: HL-60 cells were synchronized to the edge of G1 / S phase by two-step over-thymidine blocking method. Cells were harvested after treated with 5 × 10-6 mol / L retinoic acid or retinoic acid for 1d to 4d, Cell cycle phase distribution was analyzed by FCM. The expression of CyclinE, CyclinD1 and P34cdk2 protein were detected by Western blotting. Results: The expression of CyclinE and D1 protein showed a cyclic dependence. The expression of CyclinE and D1 protein increased in the G1 phase, reached the peak in the S phase and decreased in the G2 phase. However, the expression of P34cdk2 protein did not change significantly during the whole cell cycle. Most of the cells were blocked in G0 / G1 phase, P34cdk2 protein expression did not change significantly, while CyclinE and D1 protein expression decreased significantly. CONCLUSION: The decreased expression of CyclinE and CyclinD1 induced by retinoic acid or aztreonam may be related to the effect of retinoids on the G1 → S phase transition of cells, and the suppression of HL-60 cell proliferation and differentiation.