5-azacytidine induction of thymidine kinase in a spontaneously enzyme-deficient murine tumor line.
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.
D000818:Animals; D001374:Azacitidine / Q000494:pharmacology*; D002455:Cell Division; D002460:Cell Line; D004273:DNA, Neoplasm / Q000378:metabolism; D004790:Enzyme Induction; D008745:Methylation; D051379:Mice; D009374:Neoplasms, Experimental / Q000201:enzymology*; D013937:Thymidine Kinase / Q000096:biosynthesis* / Q000172:deficiency
D004273:DNA, Neoplasm; D013937:Thymidine Kinase; D001374:Azacitidine