Barfod N M, Bichel P
Virchows Arch B Cell Pathol. 1976 Sep 17;21(3):249-58. doi: 10.1007/BF02899158.
In most experimental ascites tumors the growth rate decreases with increasing age and cell number. This decrease is caused by a prolongation of the cell cycle and an increasing accumulation of noncycling cells in resting (or quiescent) G1 and G2 compartments. In cell-free ascitic fluid from the JB-1 ascites tumor in the plateau phase of growth, low molecular weight substances have been found which reversibly and specifically arrest JB-1 cells in G1 and G2. In order to characterize the JB-1 G1 inhibitor we have investigated the effect of ion exchangers and polyions on the activity of this inhibitor assayed in vitro by means of a partially synchronized JB-1 cell population analyzed by flow microfluorometry. The results indicate that polyanions and cation exchangers (immobilized polyanions) bind and abolish the G1-inhibitory activity. From this it is suggested that the G1 inhibitor is of a basic or polycationic nature. Since anion exchangers (immobilized polycations) are without effect on this activity it was surprising to find that polycations also neutralize the activity. The results indicate that this occurs by blocking an anionic G2-inhibitor receptor on the cell, thus preventing the polycationic G1 inhibitor from being bound to this receptor.
在大多数实验性腹水肿瘤中，生长速率随着年龄和细胞数量的增加而降低。这种降低是由细胞周期的延长以及静止（或静止期）G1和G2区室中非循环细胞的积累增加所引起的。在处于生长平台期的JB - 1腹水肿瘤的无细胞腹水中，已发现低分子量物质，它们能使JB - 1细胞在G1和G2期可逆且特异性地停滞。为了表征JB - 1 G1抑制剂，我们通过流式微荧光法分析部分同步化的JB - 1细胞群体，研究了离子交换剂和聚离子对体外测定的该抑制剂活性的影响。结果表明，聚阴离子和阳离子交换剂（固定化聚阴离子）结合并消除G1抑制活性。由此表明，G1抑制剂具有碱性或聚阳离子性质。由于阴离子交换剂（固定化聚阳离子）对该活性无影响，所以发现聚阳离子也能中和该活性就令人惊讶了。结果表明，这是通过阻断细胞上的阴离子G2抑制剂受体来实现的，从而阻止聚阳离子G1抑制剂与该受体结合。
