5-azacytidine induction of thymidine kinase in a spontaneously enzyme-deficient murine tumor line.
5-azacytidine induction of thymidine kinase in a spontaneously enzyme-deficient murine tumor line.
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5-氮杂胞苷在自发酶缺陷的小鼠肿瘤系中诱导胸苷激酶。
DOI：
10.1016/0014-4827(84)90596-2
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发表时间：
1984
影响因子：
3.7
通讯作者：
Kerbel,RS
中科院分区：
文献类型：
--
作者：
Liteplo,RG;Frost,P;Kerbel,RS
在我们对小鼠肿瘤细胞转移的研究过程中，发现我们的一种变异株（称为L 61-M）由于胸苷激酶（TK）活性的自发缺陷而不能将[甲基-3H]胸苷掺入DNA中。L 61-M细胞不能在HAT选择培养基中增殖，并且对溴脱氧尿苷（BrdU）具有抗性。L 61-M细胞中的TK活性是野生型亲本MDAY-D2细胞系中发现的TK活性的4.2%。用5-氮杂胞苷（一种已知的DNA低甲基化诱导剂）处理L 61-M导致TK活性的表达。这些观察结果表明，L 61-M细胞系中的TK缺陷部分是由于DNA甲基化模式的改变，导致TK基因表达减少。这些结果证明了5-氮杂胞苷在自发酶缺陷型鼠肿瘤细胞系中诱导TK活性的能力。
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.