Hamilton J A
J Cell Physiol. 1983 Apr;115(1):67-74. doi: 10.1002/jcp.1041150111.
The tumor-promoting phorbol ester, 12-0-tetradecanoyl-phorbol-13-acetate (TPA), stimulates starch-elicited mouse peritoneal macrophages to undergo DNA synthesis in vitro, apparently without the generation of an endogenous macrophage growth factor (MGF). No evidence was found for any synergistic interaction between TPA and exogenous colony stimulating factors (CSFs) for macrophage DNA synthesis. Low concentrations of glucocorticoids and also prostaglandins E1 and E2 suppress both the CSF-1-stimulated and the TPA-stimulated macrophage DNA synthesis; these same drugs inhibit the CSF-1-mediated and TPA-mediated enhancement of macrophage plasminogen activator (PA) activity. Thus glucocorticoids and prostaglandins E1 and E2 oppose the action of growth factors and the tumor promoter on macrophage and precursor cell function.
促肿瘤佛波酯12-O-十四烷酰佛波醇-13-乙酸酯（TPA）可刺激淀粉诱导的小鼠腹腔巨噬细胞在体外进行DNA合成，显然无需产生内源性巨噬细胞生长因子（MGF）。未发现TPA与外源性集落刺激因子（CSF）之间存在促进巨噬细胞DNA合成的协同相互作用。低浓度的糖皮质激素以及前列腺素E1和E2可抑制CSF-1刺激的和TPA刺激的巨噬细胞DNA合成；这些药物同样会抑制CSF-1介导的和TPA介导的巨噬细胞纤溶酶原激活剂（PA）活性增强。因此，糖皮质激素以及前列腺素E1和E2可对抗生长因子和肿瘤启动子对巨噬细胞和前体细胞功能的作用。
