Only in Titles

           Search results for: Fos Protein 1, WB control    

paperclip

#8625438   // Save this To Up

Growth modulation of hepatocytes and rat liver epithelial cells (WB-F344) by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

Modulation of DNA synthesis by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) was studied in primary cultures of hepatocytes and in rat liver epithelial cells (WB-F344) to develop models for studies on the interactions between the activated Ah receptor and cellular growth control. In hepatocytes TCDD either positively or negatively modulated EGF-stimulated DNA synthesis. In the presence of ethinylestradiol 10(-12) M TCDD moderately increased EGF-stimulated DNA synthesis (approximately 30%). In contrast, 10(-9) M TCDD in the absence of ethinylestradiol decreased DNA synthesis (approximately 30%). Analysis of variance revealed that the TCDD effects were highly significant. The response of 'early genes' of the jun/fos family and the corresponding proteins was also studied under these two conditions. In agreement with the DNA synthesis data, the level of c-Jun was increased or decreased in nuclear extracts. Furthermore, DNA binding of Jun/Fos proteins, including c-Jun and Fra-1, was decreased under conditions of mitoinhibition, while the level of Fra-1 in nuclear extracts was increased. In WB-F344 cells TCDD treatment for 44 h increased DNA synthesis 2- to 3-fold in comparison with controls, based on measuring [3H]thymidine incorporation into DNA or on determining the nuclear labeling index with bromodeoxyuridine. This effect is probably due to inhibition of high density growth arrest by TCDD. The proposed cellular models may be useful to elucidate the interactions between the activated Ah receptor and signaling pathways of growth homeostasis.

2310 related Products with: Growth modulation of hepatocytes and rat liver epithelial cells (WB-F344) by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

Epidermal Growth Factor ( Epidermal Growth Factor ( Rat growth hormone releas Rat transforming growth f glial cells missing homol Pyruvate Kinase(liver RBC alkaline phosphatase (liv GLP 1 ELISA Kit, Rat Gluc GLP 2 ELISA Kit, Rat Prog Glucagon ELISA KIT, Rat G Leptin ELISA Kit, Rat Lep Rat Insulin-like Growth F

Related Pathways

  •  
  • No related Items
paperclip

#7954458   // Save this To Up

Transforming growth factor beta 1 promotes spontaneous transformation of cultured rat liver epithelial cells.

The neoplastic transformation of cultured rat liver epithelial cells by various means has consistently been associated with the development of resistance to the mito-inhibitory effect of transforming growth factor beta (TGF-beta), suggesting that such phenotype plays a mechanistic role during the transformation of these cells. We have studied the induction of the "TGF-beta-resistant" phenotype in a clonal strain of early passage WB-F344 normal cultured rat liver epithelial cells, the proliferation of which was markedly inhibited by TGF-beta. The control WB cells in continuous culture slowly developed TGF-beta resistance. However, when the same cells were exposed to step-wise increases of TGF-beta concentration in their culture medium, the development of TGF-beta resistance was accelerated. Cells which had been grown in medium containing 1 ng/ml TGF-beta developed colony-forming capacity in soft agar containing epidermal growth factor. Cells which were grown in media containing 5 and 10 ng/ml TGF-beta demonstrated a low level of colony-forming efficiency in soft agar medium without added epidermal growth factor and tumorigenicity in isogeneic rats. These TGF-beta-resistant cells also exhibited progressively increasing levels of expression of the c-fos and and myc mRNA, and increased resistance to the cytotoxicity of Adriamycin and melphalan. The latter phenomenon was accompanied by an increase in the mdr-1 mRNA expression, cellular glutathione level, and glutathione S-transferase activity. The results suggest that chronic exposure to high concentration of TGF-beta promotes the spontaneous neoplastic transformation of cultured rat liver epithelial cells, and that this process may represent one of the mechanisms of cellular adaptation for induction of the multidrug-resistant phenotype during the carcinogenesis of epithelial cells.

2172 related Products with: Transforming growth factor beta 1 promotes spontaneous transformation of cultured rat liver epithelial cells.

Human Transforming Growth Human Transforming Growth Rat transforming growth f Rat Insulin-like Growth F Rat Vascular Endothelial Rat monoclonal anti mouse Rat monoclonal anti mouse Rat monoclonal anti mouse Rat monoclonal anti mouse Rat monoclonal anti mouse Rat monoclonal anti mouse Rat monoclonal anti mouse

Related Pathways