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目的 研究4种集落刺激因子(CSF):粒细胞集落刺激因子(G-CSF)、粒细胞-单核细胞集落刺激因子(GM-CSF)、白细胞介素-3(IL-3)和干细胞因子(SCF)对前列腺癌PC-3M细胞雄激素受体(AR)活化的途径。方法 将含人雄激素受体和雄激素受体报告基因氯霉素乙酰转移酶质粒转染至人前列腺癌细胞株PC-3M,集落刺激因子作用于转染了雄激素受体及其报告基因的细胞,对照组中同时加入终浓度为 50 mmol/L的 JAK-STAT途径持异性阻断剂 AG-490,检测外源性雄激素受体和报告基因的表达量。结果 PC-3M细胞能够表达外源性雄激素受体,10～100μg/L的G-CSF、GM-CSF、IL-3和SCF均能激活PC-3M细胞中外源性雄激素受体,检测到CAT的表达量在(0.58±0.16)μg/g到(3.80±0.89)μg/g之间,其表达量与培养基中的CSF浓度成正比;在终浓度 50 mmol/L AG-490的对照组中报告基因表达量显著下降或检测不到表达。结论 SCF能够激活PC-3M中外源性雄激素受体表达,JAK-STAT途径可能是人前列腺癌细胞雄激素受体旁路激活的机制之一。
Objective To investigate the effects of four kinds of colony stimulating factors (CSFs) such as G-CSF, GM-CSF, IL-3 and stem cell factor (SCF) on the activation of androgen receptor (AR) in prostate cancer PC-3M cells. METHODS: Human prostate cancer cell line PC-3M was transfected with human androgen receptor and chloramphenicol acetyltransferase gene, an androgen receptor reporter gene. Colony-stimulating factor was used to effect the transfection of androgen receptor and its reporter gene Cells and control group were simultaneously treated with AG-490, a JAK-STAT-specific inhibitor of STAT of JAK-STAT at a final concentration of 50 mmol / L to detect the expression of exogenous androgen receptor and reporter gene. Results PC-3M cells could express exogenous androgen receptor, and 10-100μg / L of G-CSF, GM-CSF, IL-3 and SCF could activate exogenous androgen receptor in PC-3M cells. The expression level of CAT was between (0.58 ± 0.16) μg / g and (3.80 ± 0.89) μg / g, which was proportional to the concentration of CSF in culture medium. At the concentration of 50 mmol / L AG-490 The control group showed a significant decrease in gene expression or undetectable expression. Conclusion SCF can activate exogenous androgen receptor expression in PC-3M, and JAK-STAT pathway may be one of the mechanisms of human prostate cancer bystander pathway.