F9 embryonal carcinoma cells

Imidazole antimycotics, ketoconazole, clotrimazole, and miconazole are potent inhibitors of various cytochrome P450-isoenzymes that also affect the metabolism of retinoids. They were fust shown to inhibit the metabolism of RA in F9 embryonal carcinoma cells. When tested in vitm liarazole, a potent CYP-inhibitor, suppressed neoplastic transformation and upregulated gap junctional communication in murine and human fibroblasts, which appeared to be due to the presence of retinoids in the serum component of the cell culture medium. Furthermore, liarazole magnified the cancer chemopreventive activity of RA and (3-carotene in these experiments by inhibiting RA-catabolism as demonstrated by absence of a decrease in RA-levels in the culture medium in the presence of liarazole over 48 h, whereas without liarazole 99% of RA was catabolized. In vivo, treatment with liarazole and ketoconazole reduced the accelerated catabolism of retinoids and increased the mean plasma all-irans-RA-concentration in patients with acute promyelocytic leukemia and other cancels. 

F9 embryonal carcinoma cells have a simple set of growth supplements which are required for growth in serum-free medium insulin, transferrin, and fibronectin (Rizzino and Sato, 1978). Fibronectin is a component of the extracellular matrix and facilitates the attachment of the cells to the culture dish. In addition, high density lipoprotein (HDL) has been observed to promote the growth of F9 cells serum-free. 

Hennemann H, Schwarz J, Willecke K Characterization of gap junction genes expressed in F9 embryonic carcinoma cells Molecular cloning of mouse connexin31 and -45 cDNAs. Eur J Cell Biol 1992a 57 51-58. 

H. Chiba, J. Clifford, D. Metzger, and P. Chambon. Distinct retinoid X receptor-retinoic acid receptor heterodimers are differentially involved in the control of expression of retinoid target genes in F9 embryonal carcinoma cells. Mol Cell Bid, 17 (6), 3013-3020, 1997. 

Rusciano, D., Lorenzoni, P. and Burger, M. M. (1991). The role of both specific cellular adhesion and growth promotion in fiver colonization by F9 embryonal carcinoma cells. Int. J. Cancer 48, 450-456. 

Kihara A, Ikeda M, Kariya Y, Lee EY, Lee YM, Igarashi Y (2003) Sphingosine-1-phosphate lyase is involved in the differentiation of F9 embryonal carcinoma cells to primitive endoderm. J Biol Chem 278 14578-14585... 

Espeseth, A S, Murphy, S P, and Linney, E (1989) Retinoic acid receptor expression vector inhibits differentiation of F9 embryonal carcinoma cells Genes and Dev 3,1647-1656. 

A variety of cell lines, including murine-F9 embryonal-carcinoma cells, murine-melanoma cells (B16 and S9), HeLa cells and HL-60 promyelocytic leukemia cells, have been successfully used for the extraction of RARs from nuclei (1,9). For cell lines growing as monolayers, we have used three 75-cm flasks at cell densities of 5 x 10 to 10 cells per flask for a typical experiment. In the case of HL-60 cells, which grow only in suspension culture, the cells are normally maintained at densities of 0.3 x 10 to 0.9 x 10 cells/mL but may be... 

Daly, A K. and Redfern, C. P F (1987) Characterisation of a retmoic-acid binding component from F9 embryonal carcinoma cell nuclei Eur J. Biochem 68, 133-139... 

Fujimura, F. K., Deininger, P. L., Friedman, T., and Linney, E., 1981, Mutation near the polyoma DNA replication origin permits productive infection of F9 embryonal carcinoma cells. Cell 23 809-814. 

Williams JB, Napoli JL (1985) Metabolism of retinoic acid and retinol during differentiation of F9 embryonal carcinoma cells. Proc Natl Acad ScL USA 82 4658-4662... 

To the extent that it is possible, we attempt to simplify the picture by discussing separately each of the cellular systems in which evidence exists for retinoid-mediated effects on protein kinases and protein phosphorylation. In studies of the biochemical effects of retinoids we are again faced with the central role occupied by their specific effects on neoplastic cells. The cellular systems employed for these studies have been either murine embryonal carcinoma cells (F9) or human promyelocytic leukemia cells (HL-60), each of which has been demonstrated to undergo terminal differentiation to nonneoplastic cell types following retinoid treatment (see Section IV,B,1 and 2), or murine melanoma cells in which retinoids have a marked antiproliferative effect (Section IV,B,3). 

Kondo K, Tsuneizumi K, Watanabe T, Oishi M. Induction of in vivo differentiation of mouse embryonal carcinoma (F9) cells by inhibitors of topoisomerases. Cancer Res. 50, 5398-5404, 1991. 

Terrana, B., Rusciano, D. and Pacenti, L. (1987). Organ colonization pattern of retinoic acid-treated and -untreated mouse embryonal carcinoma F9 cells. Cancer Res. 47, 3791-3797. 

Upon exposure to retinoic acid (RA), embryonal carcinoma (EC) F9 cells can be induced to differentiate into three distinct extra-embryonic types of... 

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