Perkins S L, Andreotti P E, Sinha S K, Wu M C, Yunis A A
Cancer Res. 1984 Nov;44(11):5169-75.
The human promyelocyte leukemic cell line HL-60 secretes a glycoprotein factor which stimulates HL-60 and myeloid cell growth and colony formation in vitro. Functional and biochemical studies indicate this autostimulatory activity (ASA) is distinct from colony-stimulating factor (CSF) activities reported previously. Human CSF I, CSF II, and HL-60 ASA stimulated HL-60 growth and colony formation. The ASA also demonstrated CSF activity for both granulocyte and macrophage colonies when assayed on normal mouse and human bone marrow cells. The ASA glycoprotein was partially purified 1200-fold to an apparent molecular weight of 25,000 on G-75 filtration and a pl of 4.9 after neuraminidase treatment. Serological cross-reactivity between human CSF I and HL-60 ASA was detectable by immune precipitation and neutralization of biological activity with rabbit anti-CSF I antibodies. The cross-reactive anti-CSF I antibodies also inhibited spontaneous HL-60 colony formation in vitro in the absence of exogenous CSF, ASA, or anti-HL-60 antibody activity. These results indicate that HL-60 ASA is an endogenous growth factor similar to CSF that may be required for HL-60 growth in vitro.
人早幼粒细胞白血病细胞系HL-60分泌一种糖蛋白因子,该因子在体外可刺激HL-60和髓系细胞生长及集落形成。功能和生化研究表明,这种自刺激活性(ASA)与先前报道的集落刺激因子(CSF)活性不同。人CSF I、CSF II和HL-60 ASA均可刺激HL-60生长及集落形成。当在正常小鼠和人骨髓细胞上进行检测时,ASA对粒细胞集落和巨噬细胞集落也表现出CSF活性。经G-75过滤,ASA糖蛋白被部分纯化了1200倍,其表观分子量为25,000,经神经氨酸酶处理后的pI为4.9。通过免疫沉淀以及用兔抗CSF I抗体中和生物活性,可检测到人CSF I与HL-60 ASA之间的血清学交叉反应性。在没有外源性CSF、ASA或抗HL-60抗体活性的情况下,交叉反应性抗CSF I抗体在体外也能抑制HL-60自发集落形成。这些结果表明,HL-60 ASA是一种类似于CSF的内源性生长因子,可能是HL-60体外生长所必需的。