Yamashita Y, Nara N, Aoki N
First Department of Internal Medicine, Tokyo Medical and Dental University, Japan.
Cancer Res. 1989 Oct 1;49(19):5334-8.
A variant clone was adopted during passages of a small cell lung cancer cell line, GKT3-1.3. The variant clone exhibited distinct characteristics with alterations in morphology, positive staining with nonspecific esterase stain, and an increase in surface specific markers OKM5, HLA-DR, Mo1, and My7, usually found on monocytes or their precursors. However, it exerted a very rapid proliferation just like immature cells. This new clone, GKT3-1.3V, was shown to have specific binding capacity to granulocyte-macrophage colony-stimulating factor (GM-CSF), with a number of binding sites comparable to that of myelomonocytes or monocytic cell lines. Thus its proliferation was inhibited by GM-CSF in clonogenic assay and suspension culture. Increase in the percentage of cells with surface marker Mo1 by the addition of GM-CSF suggested its differentiative effect. Cell cycle analysis showed that the antiproliferative effect of GM-CSF was due to a block in G0 or G1. The antiproliferative effect of GM-CSF was abolished by the addition of anti-GM-CSF antibody.
在小细胞肺癌细胞系GKT3-1.3传代过程中出现了一个变异克隆。该变异克隆表现出明显的特征,形态发生改变,非特异性酯酶染色呈阳性,并且表面特异性标志物OKM5、HLA-DR、Mo1和My7增加,这些标志物通常在单核细胞或其前体上发现。然而,它像未成熟细胞一样增殖非常迅速。这个新克隆GKT3-1.3V被证明对粒细胞-巨噬细胞集落刺激因子(GM-CSF)具有特异性结合能力,其结合位点数量与骨髓单核细胞或单核细胞系相当。因此,在克隆形成试验和悬浮培养中,GM-CSF可抑制其增殖。添加GM-CSF后,表面标志物Mo1的细胞百分比增加,表明其具有分化作用。细胞周期分析表明,GM-CSF的抗增殖作用是由于细胞阻滞在G0或G1期。添加抗GM-CSF抗体后,GM-CSF的抗增殖作用被消除。