Deschatrette J, Moore E E, Dubois M, Cassio D, Weiss M C
Somatic Cell Genet. 1979 Nov;5(6):697-718. doi: 10.1007/BF01542636.
Two independent dedifferentiated variants, H5 and FaoflC2, derived from the Reuber H35 hepatoma, produce trans-acting diffusible substances(s) that extinguish the expression of liver-specific proteins when hybridized with a well-differentiated cell line of the same origin (Fao and Fu5-5, respectively). H5 x Fao hybrids show total and stable extinction of four liver functions and clonal variability in the expression of three others. FaoflC2 x Fu5-5 hybrids are initially flat (like FaoflC2 cells), and die in glucose-free medium where survival requires expression of hepatic gluconeogenic enzymes, but then evolve to hepatoma-like and finally round morphology; these latter cells express all liver functions analyzed including the gluconeogenic enzymes. Two exceptional clones that remained flat long enough for complete analysis showed extinction of all hepatic functions not expressed by FaoflC2 cells. We conclude that this transitory extinction reflects the action and then loss of extinguishing factor(s) contributed by FaoflC2. When crossed with BW1-J mouse hepatoma cells. FaoflC2 causes stable extinction of mouse aldolase B. We propose that production of extinguishing factor(s) is the rule for dedifferentiated variants.
源自鲁伯H35肝癌的两个独立的去分化变体H5和FaoflC2，会产生反式作用的可扩散物质，当与同一来源的高分化细胞系（分别为Fao和Fu5-5）杂交时，这些物质会抑制肝脏特异性蛋白的表达。H5与Fao杂交体显示出四种肝功能的完全且稳定的抑制，以及另外三种肝功能表达的克隆变异性。FaoflC2与Fu5-5杂交体最初是扁平的（像FaoflC2细胞），并在无葡萄糖培养基中死亡，而在这种培养基中存活需要肝糖异生酶的表达，但随后会演变成肝癌样形态，最终呈圆形；这些后期细胞表达了所有分析过的肝功能，包括糖异生酶。两个异常克隆保持扁平状态足够长的时间以进行完整分析，结果显示所有未由FaoflC2细胞表达的肝功能均被抑制。我们得出结论，这种短暂的抑制反映了FaoflC2所贡献的抑制因子的作用，然后是其丧失。当与BW1-J小鼠肝癌细胞杂交时，FaoflC2会导致小鼠醛缩酶B的稳定抑制。我们提出，产生抑制因子是去分化变体的普遍规律。
