Guguen-Guillouzo C, Corlu A, Loyer P, Baffet G, Gripon P
INSERM U49, Hôpital de Pontchaillou, RENNES.
Ann Gastroenterol Hepatol (Paris). 1994 Mar-Apr;30(2):64-9.
The liver epoch like other tissue epochs occurs after that different events have induced heterogeneity in embryonic cells which results in distinct evolutionary processes. These events and those of organogenesis like "induction" are deeply dependent on cell-cell communications. Cell-cell interactions involve either soluble factors (hormones, growth factors), extracellular matrix or plasma membrane proteins responsible for cell-cell recognition and/or adhesion. All these plasma membrane signals are transduced to the nucleus and modulate the expression of groups of genes. To be functionally stable along the adult stage the liver has to maintain an ordered activity of cell renewal. This balance between proliferation and differentiation is, at least in part, controlled by cell-cell communications. Therefore, it is not surprising that intercellular communications are altered during hepatocarcinogenesis. They involve changes in the distribution of junctions, in the amounts of extracellular matrix components and/or growth factors which all result in modifying the differentiation/proliferation balance. Cell culture models have been used for these different studies; new in vitro systems should be set up in the near future by taking advantage of the targeted hepatocarcinogenesis in transgenic mouse.
与其他组织时期一样，肝时期发生在不同事件诱导胚胎细胞产生异质性之后，这导致了不同的进化过程。这些事件以及器官发生事件，如“诱导”，都深度依赖细胞间通讯。细胞间相互作用涉及可溶性因子（激素、生长因子）、细胞外基质或负责细胞间识别和/或黏附的质膜蛋白。所有这些质膜信号都被转导至细胞核并调节基因组的表达。为了在成年阶段保持功能稳定，肝脏必须维持细胞更新的有序活动。增殖与分化之间的这种平衡至少部分受细胞间通讯控制。因此，细胞间通讯在肝癌发生过程中发生改变也就不足为奇了。它们涉及连接分布的变化、细胞外基质成分和/或生长因子数量的变化，所有这些都导致分化/增殖平衡的改变。细胞培养模型已用于这些不同的研究；利用转基因小鼠中的靶向肝癌发生，在不久的将来应建立新的体外系统。
