Pattern of proteasome expression in Walker 256 tumor cells after their transplantation into the Brattleboro rats with genetic defect of vasopressin synthesis

• Published in: Doklady. Biochemistry and biophysics 2008-04, Vol.419 (1), p.93-97
• Main Authors: Sharova, N. P., Mel’nikova, V. I., Khegai, I. I., Karpova, Ya. D., Dmitrieva, S. B., Astakhova, T. M., Afanas’eva, M. A., Popova, N. A., Ivanova, L. N., Zakharova, L. A.
• Format: Article
• Language: English
• Subjects: Animals; Biochemistry; Biological and Medical Physics; Biomedical and Life Sciences; Biophysics; Carcinoma 256, Walker - enzymology; Carcinoma 256, Walker - genetics; Carcinoma 256, Walker - metabolism; Cell Line, Tumor; Cells; Genetic disorders; Life Sciences; Molecular Biology; Neoplasm Transplantation; Proteasome Endopeptidase Complex - metabolism; Proteasomes; Rats; Rats, Brattleboro; Rodents; Studies; Transplantation; Transplants & implants; Tumor cells; Tumors; Vasopressin; Vasopressins - biosynthesis
• ISSN: 1607-6729; 1608-3091
• DOI: 10.1134/S1607672908020129

The authors have shown previously that tumor cell growth depends of the ratio of different proteasome forms. In the growing cells of mouse ascite carcinoma Krebs-II, the expression of the constitutive 26S proteasomes is significantly higher than in cells of healthy organs, whereas the expression of immune 26S proteasomes is decreased by an order of magnitude. A large pool of the constitutive 26S proteasomes is required for regulating the cell cycle of intensely proliferating malignant cells; at the same time, a drop in the content of immune proteasomes seems to enable tumor cells to escape immune control. Nevertheless, it remains unclear to what extent malignant tumor regression depends on the proteasome pool. The line-nonspecific Walker 256 carcinosarcoma, which can grow and undergo regression in Brattleboro rats, is a convenient model for studying the above problem. The transplantable Walker 256 strain originates from a rat mammary cancer line and is sensitive to hormonal effects. Hormonal imbalance is characteristic of the Brat-tleboro rats because their arginine-vasopressin (AVP) gene is inactivated. The lack of AVP leads primarily to abnormal waterelectrolyte metabolism and is a cause of diabetes insipidus. In ontogeny of the Brattleboro rats, significant morphofunctional deviations are also observed in the immune system; these are involution of both thymus and spleen, inhibition of humoral and cellular immune response, and reduced macrophage activity. At the same time, the natural killer cell activity that plays an important role in innate anti-tumor immunity is increased in the Brattleboro rats as compared to physiologically normal animals]. Here the authors studied the dynamics of the total pool of proteasomes as well as the individual dynamics of immune proteasomes, the 19S subparticle of the 26S proteasome, and the PA28 protein activator of proteasomes in Walker 256 tumor cells at different terms after the tumor transplantation into the mutant Brattleboro rats or to the rats of normal WAG line.