Weinberg J B, Misukonis M A
Cancer Res. 1984 Dec;44(12 Pt 1):5594-8.
Various human and mouse myeloid leukemia cell lines can differentiate to mature myeloid or monocytoid cells in response to different agents. The myeloblastic leukemia of the RFM/Un mouse (the RF.AML line) was studied here to determine its ability to differentiate after in vitro and in vivo treatment. The RF.AML cells were passed in vivo by i.v. or i.p. injection of freshly harvested leukemic spleen cells or in vitro-passaged leukemia cells. The cells proliferated in the spleen and peritoneal cavity. The RF.AML cells had the appearance of myeloblasts or myelomonoblasts on Wright's stain, had slight positivity for peroxidase, and lacked staining for nonspecific esterase. The cells grew in suspension in vitro with a doubling time of 48 hr. Various phorbol diester tumor promotors inhibited proliferation and incorporation of thymidine into the RF.AML cells. Phorbol myristate acetate (10 to 100 nM) caused the cells to adhere to plastic, and enhanced the phagocytic ability of the cells for Candida albicans. The RF.AML cells had specific receptors for phorbol dibutyrate, binding 0.37 +/- 0.03 (S.E.) pmol of [3H]phorbol dibutyrate/10(6) cells after a 2-hr incubation at 4 degrees with 50 nM [3H]phorbol dibutyrate. Thirty-three to 300 nM dexamethasone caused 19 to 37% of the cells to become nonspecific esterase positive and enhanced their phagocytosis of C. albicans. Likewise, 0.5 or 1.0 microM 13-cis-retinoic acid, or 0.6 or 1.2% dimethyl sulfoxide enhanced the phagocytic ability of the RF.AML cells but had no effect on the adherence, proliferation, or nonspecific esterase activity. None of the treatments induced lysozyme activity in the cells or rendered the RF.AML cells able to produce H2O2 in response to phorbol myristate acetate treatment in vitro. In vivo treatment of mice with RF.AML present with phorbol myristate acetate or dexamethasone did not induce differentiation of the RF.AML cells or alter the survival of the animals. Thus, although the RF.AML cells differentiate in vitro in response to various agents, in vivo differentiation was not seen in this model.
多种人类和小鼠髓系白血病细胞系可响应不同因子分化为成熟的髓系或单核细胞样细胞。本研究对RFM/Un小鼠的髓母细胞白血病（RF.AML细胞系）进行了研究，以确定其在体外和体内处理后的分化能力。通过静脉注射或腹腔注射新鲜收获的白血病脾细胞或体外传代的白血病细胞，使RF.AML细胞在体内传代。细胞在脾脏和腹腔中增殖。RF.AML细胞经瑞氏染色后呈髓母细胞或髓单核母细胞形态，过氧化物酶呈弱阳性，非特异性酯酶染色阴性。这些细胞在体外悬浮生长，倍增时间为48小时。多种佛波酯肿瘤促进剂可抑制RF.AML细胞的增殖以及胸苷掺入。佛波醇肉豆蔻酸酯乙酸酯（10至100 nM）可使细胞黏附于塑料表面，并增强细胞对白色念珠菌的吞噬能力。RF.AML细胞具有佛波醇二丁酸酯的特异性受体，在4℃用50 nM [3H]佛波醇二丁酸酯孵育2小时后，每10(6)个细胞可结合0.37±0.03（标准误）pmol的[3H]佛波醇二丁酸酯。33至300 nM地塞米松可使19%至37%的细胞非特异性酯酶呈阳性，并增强其对白色念珠菌的吞噬作用。同样，0.5或1.0 μM 13 - 顺式维甲酸，或0.6或1.2%二甲基亚砜可增强RF.AML细胞的吞噬能力，但对细胞黏附、增殖或非特异性酯酶活性无影响。所有处理均未诱导细胞产生溶菌酶活性，也未使RF.AML细胞在体外经佛波醇肉豆蔻酸酯乙酸酯处理后能够产生过氧化氢。用RF.AML细胞接种的小鼠在体内接受佛波醇肉豆蔻酸酯乙酸酯或地塞米松处理后，未诱导RF.AML细胞分化，也未改变动物的存活情况。因此，尽管RF.AML细胞在体外可响应多种因子发生分化，但在该模型中未观察到体内分化现象。
