【摘要】 目的:探讨G-CSF在人实体肿瘤细胞株中的表达及外源性rhG-CSF对肿瘤细胞增殖的影响及机制。方法:人G-CSF ELISA试剂盒检测肿瘤细胞G-CSF的分泌水平,细胞计数法和MTT法检测rhG-CSF对肿瘤细胞增殖的影响,流式细胞仪分析rhG-CSF对KB细胞周期和细胞凋亡的影响,免疫细胞化学检测G-CSF受体在肿瘤细胞中的表达。结果:T-24细胞分泌大量G-CSF;rhG-CSF呈剂量依赖性促KB细胞增殖,并在质量浓度为100 ng/mL达最大值,与对照相比,差异有统计学意义(P<0.05);KB细胞表达G-CSF受体,rhG-CSF拮抗KB细胞的G0/G1期阻滞,降低KB细胞凋亡率。结论:T-24细胞表达G-CSF;rhG-CSF通过作用于KB细胞表面的G-CSF受体拮抗G0/G1期阻滞、抑制凋亡而发挥促增殖作用。更多还原

【Abstract】 Objective: To investigate G-CSF expression and rhG-CSF’s effects on cell proliferation and its mechanism in human solid carcinoma cell lines.Methods:G-CSF expression was detected by human G-CSF ELISA Kit.Cell proliferation promoted by rhG-CSF was studied by cell count and MTT.The influence of rhG-CSF on KB cell cycle and apoptosis was analysed by flow cytometry.G-CSF receptor expression was detected by immunocytochemistry. Results:Cell line T-24 produced large amount of G-CSF;rhG-CSF promoted cell line KB proliferation in a dose-dependent manner and reached its maximal effect at a concentration of 100 ng/mL(P<0.05);rhG-CSF antagonized G0/G1 phase block and reduced apoptosis rate of KB cells.Conclusion: Cell line T-24 expresses G-CSF;rhG-CSF promotes KB cell proliferation by binding its G-CSF receptor,antagonizing G0/G1 phase block and inhibiting apoptosis.更多还原