Suppression of tumorigenicity mediated by 5-azacytidine and associated with increased chromosome number

C. Walker, A. M. Matthews, J. W. Shay

Research output: Contribution to journalArticle

13 Scopus citations

Abstract

5-Azacytidine (5-azaC), a hypomethylating agent, was examined for the effect on a highly tumorigenic murine cell line, T984-15. While 20 of 20 untreated subclones of T984-15 produced tumors when injected into BALB/c nude mice, 14 of 15 T984-15 subclones that were treated for 24 hours with 5 μg 5-azaC/ml displayed suppressed tumorigenesis under identical conditions. Of the 14 clones that were suppressed, 12 were nontumorigenic and 2 showed a greatly increased latency. Chromosome analyses of 5-azaC-treated nontumorigenic clones revealed that, in contrast to untreated tumorigenic controls (median chromosome number 49-59), 9 of 10 5-azaC-treated nontumorigenic clones analyzed displayed an elevated chromosome complement (68–94 chromosomes/cell). The increase in chromosome number occurred progressively with time, following a single 24-hour 5-azaC treatment, indicating that 5-azaC was not selecting for a subpopulation of cells with an elevated chromosome complement. The evidence that the hypomethylating agent 5-azaC can suppress a cell’s tumorigenic potential and that this suppression correlates with increased chromosome number suggests that 5-azaC modulates cellular phenotypes by mechanisms that involve alterations in a cell’s chromosome complement.

Original languageEnglish (US)
Pages (from-to)695-700
Number of pages6
JournalJournal of the National Cancer Institute
Volume78
Issue number4
DOIs
StatePublished - Apr 1987

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

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