Khegay Igor I, Ivanova Ludmila N
Institute of Cytology and Genetics, Siberian Branch, Russian Academy of Sciences, Novosibirsk, 630090, Russia,
Biochem Genet. 2015 Apr;53(1-3):1-7. doi: 10.1007/s10528-015-9665-1. Epub 2015 Apr 9.
Walker 256 carcinosarcoma is a transplantable model of rat carcinoma that originally appeared spontaneously in mammary glands. The growth rate of Walker 256 carcinosarcoma in vasopressin-deficient Brattleboro rats is lower than in WAG rats and their congenic hybrids with normal vasopressin levels. Study of tumor proteins detected essential alterations. Tumor regression starting at the 14th day in Brattleboro rats was accompanied by changes in the laminin pattern. At the 21st day, the concentration of α-chains became twice as low, while β-chains of laminin showed a sixfold increase compared to the initial equimolar correlation of bands. Congenic hybrids having one active copy of the vasopressin gene to provide a physiological level of hormone against the genetic background of Brattleboro rats show the same laminin alterations as WAG rats. They demonstrated a similar moderate increase of γ-chains and threefold growth of α- and β-chains of laminin in tumor tissue. It is supposed that vasopressin may be involved in the regulation of relevant local stimuli to trigger renovation of the laminin composition in a course of growing Walker 256 carcinosarcoma.
Walker 256癌肉瘤是一种可移植的大鼠癌模型,最初自发于乳腺。血管加压素缺乏的Brattleboro大鼠体内Walker 256癌肉瘤的生长速度低于WAG大鼠及其血管加压素水平正常的同源杂种大鼠。对肿瘤蛋白的研究发现了重要改变。Brattleboro大鼠从第14天开始的肿瘤消退伴随着层粘连蛋白模式的变化。在第21天,α链浓度降至初始水平的一半,而层粘连蛋白的β链与初始等摩尔条带相关性相比增加了六倍。具有一个血管加压素基因活性拷贝以在Brattleboro大鼠的遗传背景下提供生理水平激素的同源杂种大鼠表现出与WAG大鼠相同的层粘连蛋白改变。它们的肿瘤组织中层粘连蛋白的γ链有类似的适度增加,α链和β链增长了三倍。据推测,血管加压素可能参与调节相关局部刺激,以在Walker 256癌肉瘤生长过程中引发层粘连蛋白组成的更新。