Premium
AZT‐induced hypermethylation of human thymidine kinase gene in the absence of total DNA hypermethylation
Author(s) -
Lucarelli Marco,
Palitti Franco,
Carotti Daniela,
Cianfriglia Maurizio,
Signoretti Claudia,
Bozzi Argante,
Strom Roberto
Publication year - 1996
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(96)01124-6
Subject(s) - dna methylation , dna , thymidine kinase , gene , microbiology and biotechnology , thymidine , cancer research , chemistry , biology , genetics , gene expression , virus , herpes simplex virus
Genome‐wide DNA hypermethylation induced by 3′‐azido‐3′‐deoxythymidine (AZT) has been suggested to be involved in the development of AZT resistance. We used a CD4 T‐lymphoblastoid CEM line and its AZT‐resistant MT500 variant with reduced thymidine kinase activity. Evaluation of total DNA methylation, after AZT treatment, failed to show an increase in the 5‐methylcytosine level in both parental and AZT‐resistant cells. The effect was instead observed at a more specific gene level, on the three Hpa II sites present in exon 1 of the human thymidine kinase gene. These results suggest that AZT treatment can induce site‐specific hypermethylation, even in the absence of a more general DNA hypermethylating effect.