5-Azacytidine induction of thymidine kinase in a spontaneously enzyme-deficient murine tumor line |
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Authors: | Robert G. Liteplo Philip Frost Robert S. Kerbel |
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Affiliation: | 1. Cancer Research Laboratories, Department of Pathology, Queen''s University, Kingston, Ontario, Canada K7L 3N6;2. Department of Medicine, Long Beach VAH U.S.A.;3. Departments of Medicine & Microbiology, California College of Medicine, Irvine, CA, USA |
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Abstract: | During the course of our studies on murine tumor cell metastases, one of our variant lines (called L61-M) was found to be unable to incorporate [methyl-3H]thymidine into DNA, due to a spontaneous deficiency in thymidine kinase (TK) activity. L61-M cells are unable to proliferate in HAT selection medium and are resistant to bromodeoxyuridine (BrdU). TK activity in L61-M cells is 4.2% of that found in the wild-type parental MDAY-D2 cell line. Treatment of L61-M with 5-azacytidine, a known inducer of DNA hypomethylation, resulted in the expression of TK activity. These observations suggest that the TK deficiency in the L61-M cell line was due in part to an alteration in the methylation pattern of DNA, resulting in the diminished expression of the TK gene. These results demonstrate the ability of 5-azacytidine to induce TK activity in a spontaneously enzyme-deficient murine tumor cell line. |
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Keywords: | To whom offprint requests should be addressed. Istituto di Istologia ed Embriologia Generale via A. Scarpa 14 00161 Roma Italy. |
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