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Effect of 5‐azacytidine treatment on mouse embryonal carcinoma cells
Author(s) -
Cremisi Chantal
Publication year - 1983
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.1041160209
Subject(s) - teratocarcinoma , embryonal carcinoma , microbiology and biotechnology , cell culture , antigen , biology , cellular differentiation , cell , activator (genetics) , p19 cell , gene , immunology , biochemistry , genetics , adult stem cell
Several properties of embryonal carcinoma (EC) cell lines, such as multipotent PCC4‐aza‐1 cells and nullipolent F9 cells originating from murine teratocarcinoma cells, were examined after treatment with 5‐azacytidine, which produces undermethylated DNA. Drug‐treated PCC4‐aza‐1 cells exhibited morphological changes and differentiated, whereas azacytidine‐treated F9 cells displayed no detectable morphological change. After treatment with 5 azacytidine, PCC4‐aza‐1 cells, whether or not they differentiated, as well as F9 cells, became permissive for polyoma even though both cell types are usually resistant to polyoma. In contrast, only the differentiated azacytidine‐treated PCC4‐aza‐1 cells became sensitive to SV40 infection, i.e., synthesized T antigen, despite the resistance normally shown by such cells to this viral infection. In some PCC4‐aza‐1 and F9 cells, drug treatment induced expression of H2 antigen but did not derepress plasminogen activator synthesis. These results suggest that undermethylation of certain cellular genes in PCC4‐aza‐1 and F9 cells is correlated with the establishment of Py permissivity, SV40 sensitivity, H2 antigen expression, and the triggering of a differentiation process. The relationship between the expression of these characters and differentiation is discussed.