Lehrer R I, Cohen L E, Koeffler H P
Cancer Res. 1983 Aug;43(8):3563-6.
Phorbol diesters induce macrophage-like differentiation in KG-1 and HL-60 human acute myelogenous leukemia cell lines. We developed a cloned subline of KG-1, known as KG-1a, that does not differentiate when exposed to phorbol diesters. Both KG-1 and KG-1a cells have a single class of specific high-affinity receptors for labeled phorbol-12,13-dibutyrate with a mean Kd of 1.47 +/- 0.10 (S.E.) X 10(-8) M and 0.85 +/- 0.20 X 10(-8) M for the sensitive parental KG-1 line and the resistant KG-1a subline, respectively (p less than 0.025). The number of [3H]phorbol-12,13-dibutyrate binding sites (mean +/- S.E.) per cell was 3.85 +/- 0.98 X 10(5) and 3.94 +/- 0.31 X 10(5) on KG-1 and resistant KG-1a cells, respectively. We observed no significant decrease of specific binding with time (down regulation) in either KG-1, KG-1a, or HL-60 cells, suggesting that down regulation of specific phorbol-12,13-dibutyrate binding is not critical to induction of differentiation. Our data also confirm that the presence of specific high-affinity phorbol receptors on leukemic cells does not assure that phorbol diesters can trigger their differentiation.
佛波酯可诱导KG-1和HL-60人急性髓性白血病细胞系向巨噬细胞样分化。我们培育了KG-1的一个克隆亚系，称为KG-1a，当暴露于佛波酯时它不会分化。KG-1和KG-1a细胞都有一类针对标记的佛波醇-12,13-二丁酸酯的特异性高亲和力受体，敏感的亲本KG-1细胞系和抗性的KG-1a亚系的平均解离常数（Kd）分别为1.47±0.10（标准误）×10⁻⁸M和0.85±0.20×10⁻⁸M（p<0.025）。每个细胞上[³H]佛波醇-12,13-二丁酸酯结合位点的数量（平均值±标准误）在KG-1细胞和抗性KG-1a细胞上分别为3.85±0.98×10⁵和3.94±0.31×10⁵。我们在KG-1、KG-1a或HL-60细胞中均未观察到特异性结合随时间的显著降低（下调），这表明特异性佛波醇-12,13-二丁酸酯结合的下调对分化诱导并不关键。我们的数据还证实，白血病细胞上存在特异性高亲和力佛波醇受体并不能确保佛波酯能触发它们的分化。
